Asbestos

American Thoracic Society Documents
Diagnosis and Initial Management of Nonmalignant

Diseases Related to Asbestos
This official statement of the American Thoracic Society was adopted by the ATS Board of Directors
on December 12, 2003
CONTENTS
Diagnostic Criteria and Guidelines for Documenting Them
Asbestos as a Hazard
Asbestos in Lung Tissue
Clinical Evaluation and Indicators
Symptoms
Occupational and Environmental History
Physical Examination
Conventional Imaging
Computed Tomography
Bronchoalveolar Lavage
Pulmonary Function Tests
Nonmalignant Disease Outcomes
Asbestosis
Nonmalignant Pleural Abnormalities Associated
with Asbestos
Chronic Airway Obstruction
Implications of Diagnosis for Patient Management
Actions Required before Disease Is Apparent
Actions Required after Diagnosis
Conclusions
Asbestos is a general term for a heterogeneous group of hydrated
magnesium silicate minerals that have in common a tendency
to separate into fibers (1). These fibers, inhaled and displaced
by various means to lung tissue, can cause a spectrum of diseases
including cancer and disorders related to inflammation and fibrosis. Asbestos has been the largest single cause of occupational
cancer in the United States and a significant cause of disease
and disability from nonmalignant disease. To this demonstrable
burden of asbestos-related disease is added the burden of public
concern and fear regarding risk after minimal exposure.
This statement presents guidance for the diagnosis of nonmalignant asbestos-related disease. Nonmalignant asbestos-related
disease refers to the following conditions: asbestosis, pleural
thickening or asbestos-related pleural fibrosis (plaques or diffuse
fibrosis), benign (nonmalignant) pleural effusion, and airflow
obstruction. This document is intended to assist the clinician in
making a diagnosis that will be the basis for individual management of the patient. It therefore provides overarching criteria
for the diagnosis, specific guidelines for satisfying these criteria,
and descriptions of the clinical implications of the diagnosis,
including the basic management plan that should be triggered
by the diagnosis. It is understood that disease may be present
Members of the Ad Hoc Statement Committee have disclosed any direct commercial associations (financial relationships or legal obligations) related to the preparation of this statement. This information is kept on file at the ATS headquarters.
Am J Respir Crit Care Med Vol 170. pp 691715, 2004
DOI: 10.1164/rccm.200310-1436ST
Internet address: www.atsjournals.org
at a subclinical level and may not be sufficiently advanced to be

apparent on histology, imaging, or functional studies.
One of the most important implications of the diagnosis of
nonmalignant asbestos-related disease is that there is a close
correlation between the presence of nonmalignant disease and
the risk of malignancy, which may arise from exposure levels
required to produce nonmalignant disease or mechanisms shared
with premalignant processes that lead to cancer. The major malignancies associated with asbestos are cancer of the lung (with
a complex relationship to cigarette smoking) and mesothelioma
(pleural or peritoneal), with excess risk also reported for other
sites. There is a strong statistical association between asbestosrelated disease and malignancy, but the majority of patients with
nonmalignant asbestos-related disease do not develop cancer.
On the other hand, the risk of cancer may be elevated in a
person exposed to asbestos without obvious signs of nonmalignant asbestos-related disease. However, a diagnosis of nonmalignant asbestos-related disease does imply a lifelong elevated risk
for asbestos-related cancer.
DIAGNOSTIC CRITERIA AND GUIDELINES FOR

DOCUMENTING THEM
People with past exposure to asbestos consult physicians for
many relevant reasons: to be screened for asbestos-related disease, for evaluation of specific symptoms that may relate to past
asbestos exposure (known or unsuspected), for treatment and
advice, and for evaluation of impairment. In 1986, the American
Thoracic Society convened a group of experts to review the
literature and to present an authoritative consensus view of the
current state of knowledge with respect to diagnosis of nonmalignant disease related to asbestos (2). In 2001, a new group was
convened to review and to update the 1986 criteria. This statement constitutes that committees report, completed in 2004.
The criteria formulated in this statement are intended for the
diagnosis of nonmalignant asbestos-related disease in an individual in a clinical setting for the purpose of managing that persons
current condition and future health. These general criteria are
slightly modified from those presented in 1986 (Table 1) (2):
Evidence of structural pathology consistent with asbestosrelated disease as documented by imaging or histology
Evidence of causation by asbestos as documented by the
occupational and environmental history, markers of exposure (usually pleural plaques), recovery of asbestos bodies,
or other means
Exclusion of alternative plausible causes for the findings
The rest of this statement is largely devoted to presenting
clinical guidelines required to document that each of these criteria is met. Demonstration of functional impairment is not required for the diagnosis of a nonmalignant asbestos-related disease, but where present should be documented as part of the
complete evaluation. Evaluation of impairment has been exten-
692
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 170 2004
TABLE 1. CRITERIA FOR DIAGNOSIS OF NONMALIGNANT LUNG DISEASE RELATED TO ASBESTOS

1986 Guidelines
2004 Guidelines
Comparison and Notes
Chest film (irregular opacities)
Evidence of structural change, as

demonstrated by one or more of the
following:
Imaging methods
Pathology (College of American

Pathologists)
Histology (College of American

Pathologists)
Consistent time interval
Evidence of plausible causation, as

following:
Occupational and environmental history of
exposure (with plausible latency)
Markers of exposure (e.g., pleural plaques)
Recovery of asbestos bodies
Evidence of plausible causation implies that the temporal

relationship, including latency, is plausible
Rule out other causes of interstitial fibrosis

or obstructive disease
Exclusion of alternative diagnoses
The 1986 guidelines primarily addressed asbestosis but

mentioned smoking as a cause of obstructive disease.
Implicit in the article, however, is that nonmalignant
diseases presenting similarly to asbestos-related disease
should also be ruled out
Evidence of abnormal test
Evidence of functional impairment, as

following:
Signs and symptoms (including crackles)
Functional assessment is not required for diagnosis but is part

of a complete evaluation. It contributes to diagnosis in
defining the activity of disease and the resulting impairment
Signs and symptoms are not specific for diagnosis but are
valuable in assessing impairment
The 1986 criteria admitted the possibility of obstructive
disease; the 2004 criteria address this specifically
Occupational and environmental history
Asbestos bodies or fibers in lung tissue
Crackles, bilateral, not cleared by cough

Restrictive disease
Reduced diffusing capacity
Change in ventilatory function (restrictive,

obstructive patterns in context or disease
history)
Impaired gas exchange (e.g., reduced
diffusing capacity)
Inflammation (e.g., by bronchoalveolar
lavage)
Demonstrates the existence of a structural lesion consistent

with the effects of asbestos. The criteria outlined in the 1986
guidelines were most explicit for asbestosis
Chest film, HRCT, and possibly future methods based on
imaging. The 1986 guidelines specified ILO classification 1/1
Criteria for identifying asbestosis on microscopic examination
of tissue are unchanged
The 2004 guidelines are not limited to lung tissue, consider

the role of BAL to be established, and deemphasize fibers
because they are difficult to detect and a systematic analysis
for asbestos fibers is not generally available
The 1986 guidelines noted possible utility of bronchoalveolar

lavage and gallium scanning but considered them to be
experimental techniques. The 2004 guidelines exclude
gallium scanning, suggest that additional indicators of
active inflammation may become useful in future
Exercise testing
Definition of abbreviations: BAL bronchoalveolar lavage; HRCT high-resolution computed tomography; ILO International Labour Organization.
From References 64 and 65.
sively reviewed elsewhere and is not repeated here (3). Functional impairment may be demonstrated by evidence of symptoms or signs, ventilatory dysfunction, impaired gas exchange,
and inflammation. Pulmonary function testing should be conducted in conformity with standards already published by the
American Thoracic Society (4, 5), including multiple trials to confirm reproducibility and documentation of all trials attempted.
These guidelines are designed for clinical application, not
for research, epidemiologic surveillance, screening, litigation, or
adjudication. They balance the need to be as accurate as possible
with protection of the patients safety and the yield, cost, and
accessibility of the diagnostic procedures available. These guidelines, if they err, err on the side of specificity rather than sensitivity. This is because nonmalignant asbestos-related disorders are
difficult to detect in their earliest stages and because there is no
early intervention that has been proven to alter the subsequent
evolution of the disease. On the other hand, the documentation
of causation by asbestos carries important implications for the
patient and can be established with reasonable certainty, once
the disease is identified.
Asbestos as a Hazard
The generic term asbestos is used to describe a group of

minerals that, when crushed, break into fibers. As defined by
the National Research Council (1), the term asbestos is a

commercial-industrial term rather than a mineralogical term.
It refers to well-developed and hair-like long-fibered varieties
of certain minerals that satisfy particular industrial needs. They
are chemically heterogeneous hydrated silicates and each has
chemical analogs with different structures that do not form fibers.
Fibers have parallel sides with length three or more times greater
than width. Asbestos fibers have great tensile strength, heat
resistance, and acid resistance; varieties are also flexible. The
six minerals that are traditionally defined as asbestos include
chrysotile asbestos (the asbestiform variety of serpentine); the
amphiboles, which include crocidolite (the asbestiform variety
of riebeckite) and amosite (the asbestiform variety of cummingtonite-grunerite); and the asbestiform varieties of the amphiboles, which include anthophyllite (anthophyllite asbestos), actinolite (actinolite asbestos), and tremolite (tremolite asbestos)
(6). Just as all forms of asbestos, by the definition and classification above, appear to cause malignancy, all may cause the nonmalignant diseases described. Issues of relative potency among
the forms of asbestos, and particularly between chrysotile and
the amphiboles, are primarily of concern with respect to the risk
of malignancy and are not discussed in this document.
Commercial-grade asbestos is made up of fiber bundles.
These bundles, in turn, are composed of extremely long and thin
fibers, often with splayed ends, that can easily be separated from
one another. Commercial asbestos has high tensile strength,

flexibility, resistance to chemical and thermal degradation, and
high electrical resistance, and can often be woven. On the basis
of these characteristics, asbestos was broadly used in the past
in insulation, brake linings, flooring, cement, paint, textiles, and
many other products; however, commercial use has declined
substantially in more recent years.
Asbestos and asbestiform minerals may occur as a natural
accessory mineral in other industrial mineral deposits or rocks.
These asbestiform amphiboles and some other fibrous minerals
may not completely fit the commercial definition of asbestos but
may have similar effects, such as the tremolite-like asbestiform
mineral found in association with vermiculite in Libby, Montana
(7). Although the general criteria still apply, the specific diagnostic guidelines provided in this statement may or may not apply
in such situations, depending on the mineral and exposure circumstances. Documentation of health effects in the scientific
literature for these minerals is not as extensive as for chrysotile
and the common amphiboles.
World production and use of asbestos climbed steadily since
its commercial introduction in the late nineteenth century and
fell rapidly after documentation of its hazards in the 1970s and
1980s. In Western industrialized countries, the widespread use
of asbestos in industry and in the built environment in the first
seven decades of the twentieth century has resulted in an epidemic of asbestos-related illness that now continues into the
twenty-first century, despite decline in global production and
use. Its use has now been banned in many Western countries.
Asbestos is still mined in Russia and China, mainly for local
use, and in Canada, where most of the product is exported to
Asia and Africa.
Today, with stringent regulation of asbestos use and the disappearance of almost all asbestos-containing products from the
market, nonmalignant asbestos-related disease is primarily a
concern in four settings in the developed world: (1 ) the historical
legacy of asbestos exposure affecting older workers; (2 ) the
current risk experienced by the workforce engaged in certain
occupations managing the remaining hazard, such as building
and facility maintenance; (3 ) asbestos abatement operations,
removing insulation and other asbestos-containing products; and
(4 ) renovation and demolition of structures containing asbestos.
In the developing world, workers and their families continue to
be exposed. In some countries, including industrialized countries
formerly belonging to the Eastern bloc and rapidly industrializing countries in Asia, the use of asbestos continues and may
even be increasing.
Asbestos is still a hazard for an estimated 1.3 million workers
in the construction industry in the United States and for workers
involved in maintenance of buildings and equipment (8). Most
asbestos in the United States today exists in building and machinery insulation and old products, such as appliances, that may be
available for resale. New products that may contain asbestos
today in the United States include friction surfaces (brake pads),
roofing materials, vinyl tile, and imported cement pipe and sheeting. Significant asbestos content may be present as a contaminant
in vermiculite insulation often found in homes (7).
Historically, occupations at greatest risk for nonmalignant
asbestos-related disease have tended to be those engaged in the
production and end use of products made from asbestos. These
have included a wide assortment of items, including friction pads,
brake linings, gas masks, cement water pipe, insulation, and
textiles. Occupations engaged in the mining and extraction of
asbestos have usually shown lower frequencies of nonmalignant
asbestos-related disease. Passive exposure, including workers
carrying home asbestos on their clothing, was historically associated with elevated cancer risk, particularly mesothelioma, and
693
risk of nonmalignant asbestos-related disease. Workers in building and equipment maintenance may still encounter asbestos
insulation even though asbestos is no longer widely used in
commerce. Asbestos abatement activities, including removal and
replacement of insulation, provide opportunities for exposure
among contemporary workers (8).
Asbestos in Lung Tissue
Asbestos fibers carried to the deep lung induce an alveolitis that

results in fibrosis. Inhaled asbestos fibers can also result in pleural
inflammation. Asbestos fibers are transported to the pleural surface along lymphatic channels by macrophages and/or by direct
penetration. The degree of fibrosis in asbestosis is dose dependent (912).
Asbestos fibers are deposited at airway bifurcations and in
respiratory bronchioles and alveoli primarily by impaction and
interception. Fibers migrate into the interstitium, in part via an
uptake process involving Type I alveolar epithelial cells. This
causes an alveolar macrophagedominated alveolitis, as demonstrated in Figure 1 (12, 13). Thereafter, many of the fibers are
cleared.
Activated macrophages are stimulated to engulf and remove
asbestos fibers. This process is not uniformly successful, however,
and many fibers are retained (9, 10). The long fibers cannot be
completely engulfed by the macrophage, as demonstrated in
Figure 2.
Chrysotile fibers also split longitudinally, creating additional
fibrils. These are cleared more efficiently than amphibole asbestos fibers, which may be retained indefinitely (12). The fibers
induce apoptosis, a form of controlled cell death, in the macrophage and stimulate inflammation. This effect is reduced once
the fiber is coated to create an asbestos body, but the great
majority of fibers in the lung remain uncoated. For these reasons,
asbestos has a prolonged residence in the lung, penetrates the
interstitium of the distal lung, and shows extensive mobility both
in the lung and around the body (9).
Asbestos fibers, in particular, stimulate macrophages to produce a variety of mediators. Oxygen radicals contribute to tissue
injury. Granulocytes are recruited to sites of disease activity and
they in turn release mediators that contribute to tissue fibrosis
by stimulating fibroblast proliferation and chemotaxis and ultimately promoting collagen synthesis (1115).
The inflammatory processes induced by asbestos include alveolitis, inflammation in the surrounding interstitium, and inflammation followed by fibrotic change in the respiratory bronchioles
that extends into adjacent alveolar tissue (11, 14, 16). Studies
of the lung tissue of asbestos-exposed workers, including nonsmokers, have demonstrated a form of peribronchiolitis involving the walls of membranous and respiratory bronchioles, that
shows characteristics of a more intense fibrotic response than
the small airway lesions caused by nonspecific mineral dusts that
the lesions otherwise resemble (17, 18).
Asbestos fibers and their derivatives, asbestos bodies, can
be identified and quantified in lung tissue and bronchoalveolar
lavage (BAL) specimens, as demonstrated in Figure 2 (19).
Transbronchial lung biopsy is less reliable than BAL or open
lung biopsy in recovering sufficient tissue to demonstrate elevated asbestos body or fiber counts when they do occur (20).
Asbestos fibers, unlike asbestos bodies, are rarely seen by
light microscopy and must be analyzed by scanning/transmission
electron microscopy (19, 21, 22). There is considerable variation
among laboratories in procedures to quantify asbestos fibers in
tissue (18, 23, 24), which has led to efforts to standardize procedures (19). Asbestos mineralogical types can be identified by
energy-dispersive X-ray analysis, in which detection of magnesium and silicon is characteristic of most forms of asbestos and
694
Figure 1. Low-power photomicrograph of hematoxylin and

eosin (H&E)-stained sections
from a patient with asbestosis,
showing patchy asbestosis and
a moderate number of macrophages within the alveoli. Inset:
Close-up of macrophages in an
iron-stained section showing
an asbestos body.
the presence of a large iron peak signifies an amphibole (with

the exception of tremolite) (25). Fiber analysis can be helpful
in assessment of exposure and provides information about intensity, duration, and latency (e.g., uncoated fibers may reflect recent heavy exposure). However, because some fibers dissolve over
time, the absence of a high fiber count does not necessarily mean
that there has been no exposure, especially when chrysotile is the
predominant exposure (22). Mineralogic analysis of asbestos fibers
is largely a research technique and is not widely available (26).
Asbestos bodies. Asbestos bodies are asbestos fibers that have
Figure 2. Asbestos body retrieved by bronchoalveolar lavage. Note its clear central core.
been coated with an iron-rich, proteinaceous concretion (Figures

1 and 2). Amphibole asbestos forms the majority of asbestos
bodies and is more persistent in lung tissue than chrysotile (25).
Asbestos bodies are larger than asbestos fibers and can be identified and quantified by light microscopy. An iron stain is helpful
to identify fibrous bodies coated by iron (hence the general name
ferruginous bodies). Ferruginous bodies generally form on
fibers at least 10 m in length, and more than 90% of all coated
fibers have asbestos cores. Demonstration of an elevated body
burden of asbestos confirms past exposure (19). Levels of at
least one or two asbestos bodies per field of a tissue section on
a slide under light microscopy are consistent with occupational
exposure (19, 22, 24).
Transbronchial biopsy. Transbronchial lung biopsies are usually too small to analyze for asbestos bodies. Bronchoalveolar
lavage recovers more material and therefore provides a better
indicator of tissue burden. Some experienced clinicians have
found that identification of six or more bodies in bleach-digested
samples from at least two biopsies is characteristic of patients
with occupational exposure (26). However, the absence of observable asbestos bodies is not reliable in excluding significant
exposure in transbronchial biopsy tissue (20).
These indicators of fiber burden are sufficient but not necessary to identify occupational exposure and to diagnose asbestosrelated disease. Beyond clinical research, the method has applications in litigation and exposure assessment for epidemiology.
Bronchoalveolar lavage. Asbestos bodies and fibers can be
identified and quantified in BAL specimens, as in Figure 2 (22).
There is considerable variation among laboratories in these tests
(18, 19, 22, 23). The count of asbestos bodies in BAL fluid
appears to correlate with the presence or degree of fibrosis in
some studies but not others (24, 27, 28).
BAL in patients with asbestosis has demonstrated an alveolar
macrophage alveolitis associated with a modest increase in neutrophils (12, 13). This neutrophilia correlates with the finding of crackles (rales) on physical examination and disturbances in oxygenation (12, 27) and is apt to be more pronounced in patients with
advanced disease (13). Clinically apparent asbestosis occurs only
after a significant latent period. However, studies using BAL,
computed tomography (CT) scanning, and gallium-67 scanning
have demonstrated that inflammatory events occur well before
the onset of clinical disease. Thus, it is likely that the initial
exposure induces inflammation and injury that persist through
the latent or subclinical phase and later develop into the clinical
disease, which is typically diagnosed by chest imaging (13).
CLINICAL EVALUATION AND INDICATORS

The clinical evaluation of nonmalignant asbestos-related disease
should consider subjective symptoms as well as objective findings
on physical examination, pulmonary function tests, and chest
radiographic studies. In the large majority of patients, the diagnosis of nonmalignant asbestos-related lung disease is based
on the clinical findings discussed below, in the context of an
appropriate history of exposure to asbestos and a documented
latency period sufficient to place an individual at risk.
Symptoms
The insidious onset of dyspnea is the most common respiratory

symptom associated with asbestosis, typically beginning with
dyspnea on exertion. A nonproductive cough is commonly present. The presence of wheeze or dyspnea (27), as reported on
the ATS-DLD-78A respiratory questionnaire (5), is strongly
associated with diminished ventilatory capacity in cross-sectional
studies of asbestos-exposed workers, with an 11 to 17% reduction
in ventilatory capacity (27, 29). A 28% reduction in ventilatory
695
capacity has been observed for cough, phlegm, and symptoms

of chronic bronchitis among asbestos-exposed workers (29). Development or progression of respiratory symptoms has been
associated with accelerated loss of ventilatory capacity in a longitudinal investigation of asbestos-exposed workers, with an excess
28-ml/year decline in FEV1 associated with development of dyspnea, and 67-ml/year excess decline in FVC associated with newly
developed wheezing, relative to asymptomatic individuals (30).
In a study of 64 patients, diffuse pleural thickening or fibrothorax was associated with dyspnea on exertion, usually mild,
in 95%, chest pain in more than half, and restrictive defect in
one-third. The chest pain was intermittent in most but constant
in 9% (31). Rapidly progressive or severe chest pain should
raise clinical suspicion of either malignancy or a nonmalignant
pleuritis.
Subjective symptoms are not easily interpreted in the absence
of objective findings but provide important ancillary information.
The persistence or new onset of respiratory symptoms is correlated with accelerated loss of lung function in asbestos-exposed
workers and therefore may predict future risk (30).
Occupational and Environmental History
It is essential to take a comprehensive occupational and environmental history when asbestos-related disease is suspected (32).
The occupational history should emphasize occupational and
environmental opportunities for exposure that occurred about
15 years and more before presentation.
The diagnosis of asbestosis is ideally based on an accurate
exposure history, obtained whenever possible directly from the
patient, that defines the duration, intensity, time of onset, and
setting of exposure experienced by the patient. Patients may
forget short periods of employment, during which intense exposure is possible, or employment early in their lives. In such cases
the characteristic radiographic signs of asbestos exposure may
be enough to document exposure.
The occupational title is not enough, as the names of many
occupations and trades are uninformative, such as millwright
or fireman (a misleading title that sometimes refers to furnace
workers and stokers) or mixer. Representative occupational
exposures include, but are not limited to, manufacture of asbestos products, asbestos mining and milling, construction trades
(including insulators, sheet metal workers, electricians, plumbers, pipefitters, and carpenters), power plant workers, boilermakers, and shipyard workers.
Asbestosis is commonly associated with prolonged exposure,
usually over 10 to 20 years. However, short, intense exposures
to asbestos, lasting from several months to 1 year or more, can
be sufficient to cause asbestosis. For example, shipyard workers
who applied or removed insulation in confined spaces have developed asbestosis after brief periods of heavy exposure. Insulation workers have had similarly intense exposures during their
apprenticeship when they unloaded asbestos-containing sacks
into troughs for mixing asbestos cement. Such occupational exposures are now rare but were common in the United States
from the years after World War II until the 1970s. Adequate
industrial hygiene controls were absent or not widely applied.
Protective regulations were inadequate and only partially enforced during much of that period.
Workers whose own jobs may not require handling asbestos
may still be bystanders who worked in close proximity to other
users, especially in the construction trades, where workers have
experienced exposure from insulation being installed around
them. Among sheet metal workers, for example, the prevalence
of asbestos-related changes on chest film was 31% (19% pleural
only, 7% parenchymal only, and 6% both). Among those who
had been in the trade for 40 or more years, 41.5% had radio-
696
graphic findings (33). These findings established that sheet metal

workers, although not working directly with asbestos, had substantial exposure in the work environment.
Measures taken to protect workers, or lapses in these measures, may be important in documenting exposure. Although
exposure levels are generally low in developed countries today,
lapses occur and were more frequent in the past. Some patients
who have immigrated may have worked in countries where occupational health regulations have been poorly enforced or where
environmental exposure has occurred.
Environmental sources of exposure, for example, tailings of
asbestos mines or prolonged exposure in buildings with exposed
sources of asbestos contamination, may be important in some
cases. Passive exposure, for example, of children in the home
when asbestos is brought into the house on the clothes of a
worker, may cause disease (34). Undisturbed and nonfriable
asbestos insulation in buildings, including schools, does not present a hazard.
The prevalence of asbestosis among asbestos workers increases with the length of employment, as illustrated in an early
report in which investigators analyzed chest films of 1,117 New
York and New Jersey asbestos insulation workers. They found
asbestosis in 10% of workers who had been employed for 10 to
19 years, 73% among those employed for 20 to 29 years, and in
92% of those employed for 40 or more years (35). A similar
exposureresponse relationship was found among asbestos cement workers (36).
Differences in solubility among the various types of asbestos
may affect fiber retention, body burden, and the risk of nonmalignant disease. The clinician is rarely in a position to evaluate this
aspect of exposure and there is no validated means to adjust the
occupational history to take this factor into account. Solubility
is primarily of concern with respect to projecting future risk,
particularly of malignant disease, given a history of exposure.
It is irrelevant to diagnosis when disease is already present and
other indicators of exposure are demonstrable.
Physical Examination
Physical findings in asbestosis include basilar rales, often characterized by end-inspiratory crackles (rales) (36, 37); in some cases
of advanced asbestosis, finger clubbing may be present. Physical
findings of crackles, clubbing, or cyanosis are associated with
increased risk for asbestos-related mortality (36). Although these
physical signs are useful when present, their overall clinical utility
is limited by low sensitivity. For example, in one study as many
as 80% of individuals with radiographic asbestosis demonstrated
crackles, a frequency that appears to be unusually high in the
experience of other clinicians (27).
Conventional Imaging
The chest radiograph remains an extremely useful tool for the

radiographic diagnosis of asbestosis and asbestos-related pleural
disease, and is widely available internationally. The plain film
has long been the basis for assessing asbestos-related disease
of the lung and pleura. A standardized system for taking and
classifying films for presence and profusion of opacities consistent with pneumoconiosis and for pleural changes was developed
in the 1950s and is now known as the International Classification
of Radiographs of Pneumoconiosis (or ILO classification after
its sponsor, the International Labour Organization). The ILO
classification has been revised (38). This system, which is the
basis of the B-reader qualification for designating persons as
competent in classifying pneumoconiosis films, was developed
for grading the radiographic severity of pneumoconiosis in epidemiologic studies but has been applied to clinical settings to maintain consistency in classifying chest films. The ILO classification
requires conventional film-based posteroanterior (PA) chest

films taken at prescribed specifications and classified with due
regard for quality. Conventions for classifying digitized films
and other advanced imaging systems have lagged behind the
development of technology.
The initial radiographic presentation of asbestosis is typically
that of bilateral small primarily irregular parenchymal opacities
in the lower lobes bilaterally. Over time, the distribution and
density or profusion of opacities may spread through the middle and upper lung zones. Although irregular opacities are most
common from asbestos exposure, mixed irregular and rounded
opacities are often present. The ILO classification profusion
score correlates strongly with mortality risk (36), reduced diffusing capacity, and diminished ventilatory capacity (37, 39). A
critical distinction is made between films that are suggestive but
not presumptively diagnostic (0/1) and those that are presumptively diagnostic but not unequivocal (1/0). This dividing point
is generally taken to separate films that are considered to be
positive for asbestosis from those that are considered to be
negative. However, profusion itself is continuous (36, 38).
Plain chest radiographs are limited with respect to sensitivity
and specificity in cases of mild or early asbestosis. Among individuals with asbestosis confirmed by histopathologic findings,
1520% had no radiographic evidence of parenchymal fibrosis
in one study (40), similar to the proportion of other interstitial
lung diseases that present with normal chest films (41).
Pleural plaques are frequently documented on plain chest
radiographs, but CT is more sensitive for their detection. Only
50 to 80% of cases of documented pleural thickening demonstrated by autopsy, conventional CT, or high-resolution CT
(HRCT) are detected by chest radiograph (42, 43). Plain chest
radiographs are also limited by specificity in cases of mild pleural
disease, which may be difficult to distinguish from extrapleural
fat pads (39, 44). Oblique views can enhance both sensitivity
and specificity of plain chest radiographs in clinical settings
where HRCT is unavailable, but may also fail to distinguish
plaques from fat pads (45). CT and HRCT are discussed in the
next section.
Computed Tomography
A chest film clearly showing the characteristic signs of asbestosis

in the presence of a compatible history of exposure is adequate
for the diagnosis of the disease: further imaging procedures are
not required. Conventional CT is superior to chest films in identifying parenchymal lesions, rounded atelectasis, and pleural
plaques (46). However, conventional CT has been displaced by
HRCT for the evaluation of asbestos-exposed subjects because
the latter is more sensitive for detecting parenchymal fibrosis.
In subjects with low profusion categories of asbestosis, CT
signs tend to be clustered as follows (47):
Honeycombing and thickening of septa and interlobular
fissures, suggesting interstitial fibrosis
Diffuse pleural thickening, parenchymal bands, and rounded
atelectasis, suggesting diffuse fibrosis involving the visceral
pleura
Pleural plaques
HRCT has an important role when experienced readers
disagree about the presence or absence of abnormalities on a highquality chest film, when chest radiographic findings are equivocal, when diminished pulmonary function is identified in association with otherwise normal plain chest radiographic findings,
and when extensive overlying pleural abnormalities do not allow
a clear interpretation of parenchymal markings. Because HRCT
is more sensitive than other techniques for detecting parenchymal
changes, it may reveal abnormalities with uncertain prognostic
significance. HRCT is more specific than plain chest radiographs,

excluding conditions such as emphysema, vessel prominence,
overlying pleural disease, and bronchiectasis, which may confound
radiographic interpretation.
HRCT is much more sensitive in the detection of asbestosis
than plain chest radiographs (46, 48), although even a normal
HRCT cannot completely exclude asbestosis (49). Among asbestos-exposed individuals with unremarkable chest radiographic
findings (ILO score 0/0 or 0/1), 34% were identified by HRCT
as having findings suggestive of asbestosis. HRCT findings also
correlated with decrements in pulmonary function tests in these
cases, with a significantly diminished vital capacity and diffusing
capacity (50).
HRCT can detect early pleural thickening (i.e., 12 mm in
thickness) much more sensitively than plain chest radiographs.
Pleural thickening is frequently discontinuous and interspersed
with normal regions. It is usually bilateral but may be unilateral
in a third of cases (48). HRCT also offers an advantage over
plain chest radiographs in specificity, being able to distinguish
pleural disease from extrapleural fat (51).
HRCT should be obtained at 2-cm intervals, to allow a more
accurate assessment of pleural abnormalities, as well as other
abnormal findings such as pulmonary masses (52). Prone views
should always be obtained, as it is essential to distinguish between dependent atelectasis and parenchymal fibrosis in the
posterior lung fields. HRCT findings in asbestosis are typically
bilateral, and include evidence of fibrosis (e.g., intralobular interstitial thickening and interlobular septal thickening), subpleural
dotlike opacities, subpleural lines, parenchymal bands, occasionally ground-glass opacity, and honeycombing in advanced
disease (47, 52, 53). A proposal has been put forward for a
classification system analogous to that of the ILO system for
plain chest radiographs (54), but none has been widely adopted.
The extent of plaque formation does not correlate with cumulative asbestos exposure and thus cannot be used to estimate
exposure (55).
Bronchoalveolar Lavage
Sputum analyses for asbestos bodies miss almost half of occupationally exposed individuals in whom asbestos bodies are found
on BAL (56). Thus, on the rare occasions in which the diagnosis
of asbestosis hinges on demonstration of asbestos bodies and
fibers to document exposure, BAL should be performed if sputum analysis is negative (19). Subjects with long-term exposure
have higher concentrations of fibers than those with more recent
exposure, probably because of higher workplace exposures in
the past (19).
Asbestos bodies (ABs) in BAL fluid correlate with occupational exposure and asbestosis (10, 19, 56, 57) and with asbestos
bodies in the lung (57). Patients with asbestosis consistently have
2 to 5 orders of magnitude more ABs per milliliter than do
pleural plaque subjects. Recovery of more than 1 AB/ml indicates a high probability of substantial occupational exposure to
asbestos (19, 58). In one large series, patients with asbestosis
had a log mean of 120 AB/ml, those with pleural plaques had
5 AB/ml, those exposed to asbestos who had a normal chest
X-ray had 4 AB/ml, and those with malignant mesothelioma or
lung cancer had 8 AB/ml. Of those with more than 100 AB/ml,
60% had asbestosis; others had pleural plaques, mesothelioma,
or lung cancer, and only 6% were exposed but had no evidence
of pathology (59).
BAL cells can also be digested with bleach and the residue
analyzed by electron microscopy, with fibers expressed per 106
alveolar macrophages (58). In U.S. asbestos insulation workers,
electron microscopy identified 1 chrysotile fiber in every 35 alveolar macrophages and 1 amosite fiber per 215 macrophages, with
697
no crocidolite detected. BAL performed on asbestos-exposed

subjects has recovered 28 103 fibers compared with 1 103 in
unexposed subjects (60). For every 100 fibers, there is typically
1 asbestos body (61). Clinically, the appearance of fibers or
beaded fibers on a single centrifuged BAL sample mounted
on a Diff-Quik slide represents an indicator of parenchymal
asbestosis (28).
Amphibole fiber recovery on BAL correlates well with amphibole fiber burden in the lung, but the relationship does not
hold for chrysotile because of translocation, clearance, and dissolution (57, 6163).
Pulmonary Function Tests
Evaluation of subjects with suspected asbestos-related disease

should include spirometry (with a hard copy of the flowvolume
loop for the permanent medical record), all lung volumes, and
the carbon monoxide diffusing capacity. Care should be taken to
discriminate among effects due to asbestosis, chronic obstructive
pulmonary disease, and restrictive changes due to obesity.
As with other interstitial lung diseases, the classic finding
in asbestosis is a restrictive impairment. Mixed restrictive and
obstructive impairment is frequently seen; isolated obstructive
impairment is unusual. Restrictive impairment may also be observed with pleural disease (see section on pleural abnormalities
below).
In addition to diminished lung volumes, the carbon monoxide
diffusing capacity is commonly reduced due to diminished alveolarcapillary gas diffusion, as well as ventilationperfusion mismatching. Although a low diffusing capacity for carbon monoxide is often reported as the most sensitive indicator of early
asbestosis, it is also a relatively nonspecific finding.
Exercise testing is generally not required for diagnostic purposes, but may be useful in assessing aerobic work capacity in
selected cases, or when the degree of dyspnea correlates poorly
with objective pulmonary function measurements.
NONMALIGNANT DISEASE OUTCOMES

Asbestosis
Asbestosis is the interstitial pneumonitis and fibrosis caused by

inhalation of asbestos fibers. After asbestos exposure, asbestosis
becomes evident only after an appreciable latent period. The
duration and intensity of exposure influence the prevalence of
radiographically evident parenchymal pulmonary fibrosis. In
work sites around the world that meet recommended control
levels, high exposure to asbestos is now uncommon and clinical
asbestosis is becoming a less severe disease that manifests itself
after a longer latent interval.
Asbestosis specifically refers to interstitial fibrosis caused by
the deposition of asbestos fibers in the lung (Figure 3). It does
not refer to visceral pleural fibrosis, the subpleural extensions of
fibrosis into the interlobular septae or lesions of the membranous
bronchioles.
The College of American Pathologists has developed histologic criteria for asbestosis and a grading system to describe the
severity and extent. The mildest (Grade I) form of asbestosis
involves the alveolated walls of respiratory bronchioles and the
alveolar ducts (Figures 4 and 5). More severe histologic grades
involve greater proportions of the acinus (Grade II) until the
whole acinar structure is involved (Grade III asbestosis) and
some alveoli are completely obliterated (Figure 5). Alveolar
collapse, with fibrosis and honeycomb remodeling resulting in
new dilated spaces in the parenchyma, results in the most severe
grade of asbestosis (Grade IV) (64, 65) (Figure 6). These patterns
of acinar fibrosis together with the demonstration of asbestos
bodies in standard histologic sections are diagnostic of asbestosis.
698
Figure 3. H&E-stained section

demonstrating asbestos bodies
within alveolus of person with
asbestosis. At center is a single
large asbestos body within a
multinucleated giant cell.

showing junction of terminal
(membranous) bronchiole with
a respiratory bronchiole from a
person with asbestosis who
was an ex-smoker. The walls of
the bronchioles are thickened
by collagen and show mild
smooth muscle hyperplasia.
There is a mild chronic inflammatory cell infiltrate in the wall.
These features are consistent
with asbestos-related small airway disease.
699
Figure 5.
Photomicrograph
showing predominantly Grade
III asbestosis, partially defined
by diffuse interstitial fibrosis extending from acinus to acinus.
The respiratory bronchiole at
bottom left (*) could be classified as a Grade I lesion (see
Table 2).

of lung showing Grade IV asbestosis with honeycombing.
The overlying pleura (bottom
right) is also thickened.
700
TABLE 2. HISTOLOGIC GRADES OF ASBESTOSIS
Grade
Grade of severity
0
1 or I
2 or II
3 or III
4 or IV
Grade of extent
A or 1
B or 2
C or 3
Change
No fibrosis associated with bronchioles
Early fibrosis involving walls of at least one respiratory bronchiole, with or without extension into septa
of adjacent alveoli; fibrosis confined to alveolated walls of respiratory bronchioles and ducts and not
present in more distant alveoli. Alveolitis and inflammation similar to that caused by cigarette smoking
More severe fibrosis involving acinus: alveolar ducts and/or two or more layers of adjacent alveoli. Normal
lung remains in a zone between adjacent bronchioles
Fibrosis advanced and coalescent, involves entire acinus; all lung between at least two adjacent bronchioles
is affected. Some alveoli are completely obliterated
Honeycomb remodeling and large (up to 1 cm) dilated spaces grossly visible in parenchyma
Only occasional bronchioles are involved. Most appear normal
More than occasional but less than half of bronchioles are involved
More than half of bronchioles are involved
Developed in 1980 by a committee of the College of American Pathologists.
Iron stains may facilitate recognition of the asbestos bodies;

however, the presence of asbestos bodies alone is not sufficient
to establish the diagnosis of asbestosis. Asbestosis is associated
with a variable degree (usually mild) of chronic inflammation
and increased numbers of alveolar macrophages, including multinucleate giant cells. The grades of asbestosis correlate with counts
and frequencies of asbestos fibers and bodies in the lung and
estimates of cumulative workplace exposure (12, 66) (Table 2).
Only the more severe grades of asbestosis are detectable by
gross examination. In its classic form, there is diffuse, bilateral,
pale, firm fibrosis most severe in the peripheral zones of the
lower lobes. Honeycomb cysts and areas of confluent fibrosis may
be present (Figure 7). Milder forms of asbestosis and asbestosassociated small airway disease may not be apparent to gross
inspection or to palpation, hence the importance of adequate
sampling for histology. This should include peripheral and central areas of all lung lobes (depending on the specimen) as well
as portions of visibly diseased lung. Adequate sampling of lung
adjacent to resected tumors is particularly important and frequently overlooked or inadequately sampled by pathologists. It is
strongly recommended that, when biopsy is performed, thoracic
surgeons specifically request additional sampling of lung parenchyma in resected lung specimens from patients with known or
suspected asbestos exposure (64, 65).
Asbestosis is more prevalent and more advanced for a given
duration of exposure in cigarette smokers, presumably because
of reduced clearance of asbestos fibers in the lung (67). Some
studies suggest that smokers without dust exposure may show
occasional irregular radiographic opacities on chest film, but if
so the profusion is rarely as high as 1/0; smoking alone therefore
does not result in a chest film with the characteristics of asbestosis
(68). Both smokers and ex-smokers have a higher frequency of
asbestos-related irregular opacities on their chest radiographs
than do nonsmoking asbestos-exposed workers in all profusion
categories (6870). Smoking does not affect the presentation of
asbestos-related pleural fibrosis.
Clinical diagnosis. Asbestosis is asbestos-induced pulmonary
parenchymal fibrosis, with or without pleural thickening. To
diagnose this disorder, one must establish the presence of pulmonary fibrosis and determine whether an exposure has occurred
that is of sufficient duration, latency, and intensity to be causal.
Asbestosis becomes evident only after an appreciable latency
period, often two decades under current conditions in the United
States. In one study of former workers from an amosite asbestos
insulation factory that had high levels of asbestos dust, employment for as little as 1 month resulted in a prevalence of 20% of
parenchymal opacities 20 years after exposure ceased (70). The
duration and intensity of exposure probably influence the length

of the latency period: relatively short-term, high-intensity exposures may be associated with a shorter latency than prolonged,
lower intensity exposures.
Asbestosis is usually associated with dyspnea, bibasilar rales,
and changes in pulmonary function: a restrictive pattern, mixed
restrictiveobstructive pattern, and/or decreased diffusing capacity. The abnormal PA chest film and its interpretation remain the
most important factors in establishing the presence of pulmonary
fibrosis (Figure 8). Compensation systems may require that the
chest radiographs be classified by the ILO system once it is
established that the patient has been exposed to asbestos. A
profusion of irregular opacities at the level of 1/0 is used as the
boundary between normal and abnormal in the evaluation of
the film, although the measure of profusion is continuous and
there is no clear demarcation between 0/1 and 1/0 (Figure 9).
When radiographic or lung function abnormalities are indeterminate, HRCT scanning is often useful in revealing characteristic
parenchymal abnormalities as well as correlative pleural changes
that are highly suggestive of asbestos exposure, particularly when
they are bilateral. The specificity of the diagnosis of asbestosis
increases with the number of consistent findings on chest film,
the number of clinical features present (e.g., symptoms, signs, and
pulmonary function changes), and the significance and strength
of the history of exposure.
Although asbestosis is characteristically most advanced and
appears earliest in the lower lung fields, there is a rare but wellcharacterized syndrome of massive bilateral upper lobe fibrosis,
in the absence of tuberculosis or lung cancer (7173).
The characteristic change in pulmonary function observed in
asbestosis is a restrictive impairment, characterized by reduction
in lung volumes (especially the FVC and total lung capacity),
decreased diffusing capacity, and arterial hypoxemia (74, 75).
Large airway function, as reflected by the FEV1 /FVC ratio, is
generally well preserved. In one of the earliest studies conducted,
about 50% of asbestos workers presented with FVC below 80%
predicted. The frequency of abnormal vital capacity increased,
and the mean vital capacity decreased by 18% over the subsequent 10 years (33, 75). The frequency and magnitude of the
restrictive defect increased with ILO category (i.e., increased
profusion of irregular opacities) and the presence of pleural
changes.
Notwithstanding the predominantly parenchymal and restrictive pattern of the disease, airway obstruction can also be observed and can be seen alone in nonsmokers who have asbestosis.
These patients usually have a restrictive pattern of lung function,
but clinically they also feature an obstructive component charac-
701
Figure 8. Advanced asbestosis (details of case not available). Note characteristic features: fibrotic bands superimposed on a background of
widespread irregular opacities, shaggy heart border and septal thickening, extensive pleural changes, and blunted costophrenic angles.
diagnosis of asbestosis when a significant exposure history is

obtained, lung biopsy may be warranted to exclude other, potentially treatable diseases. Biopsy material may be helpful in identifying the nature of a disease in an indeterminate case or one
lacking an adequate exposure history.
The presence of asbestos bodies in tissue sections should be
Figure 7. Whole lung section of freeze-dried lung from a person who

died of asbestosis. Note the peripheral honeycombing, which is most
severe in the lower zones.
terized physiologically by increased isoflow volume, and increased

upstream resistance at low lung volumes (14, 16). These obstructive findings may be due to asbestos-induced small airway disease. Thus, mixed restrictive and obstructive abnormalities do
not rule out asbestosis or necessarily imply that asbestos has not
caused an obstructive functional impairment (76).
Asbestosis may remain static or progress; regression is rare
(77). The factors that determine prognosis and evolution of the
disease are poorly understood. Progression, after cessation of
exposure or reduction to current permissible exposure levels, is
considerably more common in persons who already have radiographic abnormalities and appears to be associated with level and
duration of exposure and therefore cumulative exposure (78).
Differential diagnosis. Although not usually necessary for the
Figure 9. Early asbestosis, showing irregular opacities in lower lung

fields that may be categorized as 0/1 or approaching 1/0 according to
the ILO classification. Note pleural changes.
702
sufficient to differentiate asbestosis from other forms of interstitial fibrosis. The chance of finding one asbestos body from background exposure alone has been shown to be about 1 per 1,000
(79). Conversely, the presence of interstitial fibrosis in the absence of asbestos bodies is most likely not asbestosis, although
rare cases of pulmonary fibrosis with large numbers of uncoated
asbestos fibers have been described (8082). Idiopathic pulmonary fibrosis (IPF in clinical terms or usual interstitial pneumonitis in terms of pathology) has an acinar pattern of fibrosis different from that of asbestosis and is not associated with asbestos
bodies in tissue sections. On occasion, asbestosis is seen in conjunction with an unrelated interstitial lung disease (such as sarcoidosis) or in association with another pneumoconiosis, for
example, silicosis. In the absence of fibrosis, asbestos bodies are
an indication of exposure, not disease.
Asbestosis resembles a variety of other diffuse interstitial
inflammatory and fibrotic processes in the lung and must be
distinguished from other pneumoconioses, IPF, hypersensitivity
pneumonitis, sarcoidosis, and other diseases of this class. The
clinical features of asbestosis, although characteristic, are not
individually unique or pathognomonic, but the characteristic
signs of the disease are highly suggestive when they occur together. The presence of pleural plaques provides useful corollary
evidence that the parenchymal process is asbestos related.
Diagnostic uncertainty is most likely in certain groups of
patients. Patients may have a heavy cigarette-smoking history
and concurrent emphysema (which also reduces the diffusing
capacity). In such cases, one expects a history of asbestos exposure commensurate with the degree of disease. On occasion, a
patient with another interstitial lung disease, such as IPF, will
have a history of asbestos exposure. Rapid progression, with a
visible, year-to-year increase in symptoms, progression of radiographic findings, and loss of pulmonary function in the absence
of intense asbestos exposure, suggests the diagnosis of IPF rather
than asbestosis.
Patients may be exposed at various times in their working
life to more than one dust, such as silica and asbestos, or to
mixed exposures, such as dusts in combination with fumes and
vapors in welding (83). These patients may have combined disease or the effects of one dust or other exposure may dominate.
For example, predominantly upper lobe rounded opacities, hilar
node enlargement, and progressive massive fibrosis are not features of asbestosis and if present suggest other causes for the
lung disease than asbestos, such as silicosis.
On occasion, isolated fibrotic lesions associated with asbestos
resemble solitary pulmonary nodules. These are sometimes
called asbestomas and usually occur against a background of
irregular opacities; they rarely appear in isolation. They normally
require biopsy because they are not distinguishable from lung
malignancies otherwise (84).
Nonmalignant Pleural Abnormalities Associated
with Asbestos
Pleural abnormalities associated with asbestos exposure are the

result of collagen deposition resulting in subpleural thickening,
which may subsequently calcify, and which in the visceral pleura
may be associated with parenchymal fibrosis in adjacent subpleural alveoli (Figures 10 and 11). Pleural thickening, as a marker
of asbestos exposure, has continued to be a prominent feature
of exposure to asbestos while other outcomes, such as asbestosis,
have become less frequent due to declining exposure levels. The
major determinant of pleural thickening is duration from first
exposure (70).
It is unclear whether the relative frequency of diffuse and
circumscribed pleural thickening has changed. The International
Classification of Radiographs of Pneumoconioses (38) provides
a basis for recording and classifying both types of pleural thickening, allowing correlation with indices of exposure and measurements of lung function. Manifestations of disease of the lung
and of the pleura have become less evident and less characteristic
on plain films as exposures have decreased. However, CT scan
(including high-resolution images) detects pleural thickening not
evident on the plain film, and sometimes fails to confirm apparent
pleural thickening read on the plain film. Schemes to quantify
extent of pleural thickening on CT scan have been published
(55, 85). Rarely, interlobar pleural thickening may mimic lung
nodules on CT scan (86).
Pleuritis: acute pleural effusion, chronic pleuritic pain. Asbestos may cause an acute pleural effusion, often lasting several
months, that is exudative and often hemorrhagic, with variable
numbers of erythrocytes, neutrophils, lymphocytes, mesothelial
cells, and often eosinophils (8789). It may occur early (within
10 years, unlike other asbestos-related diseases) or late after the
onset of asbestos exposure (90). It may be superimposed on
long-standing pleural plaques (91). Although it is usually asymptomatic, the acute pleural effusion due to asbestos may also be
exuberant, with fever and severe pleuritic pain. It is sometimes
detected only incidentally on a radiograph taken for another
purpose (87, 88). The effusion may persist for months, present
bilaterally, or recur on the same or the opposite side (87). A
friction rub may be present (92, 93). The traces of pleural effusion
may be observed years later as a blunted costophrenic angle or as
diffuse pleural thickening. Acute pleuritis is thought to underlie
many cases of diffuse pleural thickening. Of 20 insulators with a
past history of definite pleural effusion, diffuse pleural thickening
was detected on radiograph in 16 (90). Doseresponse relationships or characteristic features of exposure associated with effusion have not been described.
Chronic severe pleuritic pain is rare in patients with asbestosrelated pleural disease (92, 93). Vague discomfort appears to be
more frequent. Studies examining the frequency of atypical chest
pain in asbestos-exposed patients have not been performed. In
the few cases described, it was present for many years, disabling,
and often bilateral. Radiographic evidence of pleural disease
ranged from plaques to extensive diffuse and circumscribed pleural thickening; several cases followed pleural effusions. The diagnosis of acute asbestos-related pleural effusion is by exclusion
of other causes of acute pleuritis, and most often is not arrived
at until the pleural space is fully explored and biopsied, generally
by thoracoscopy. Differentiation from Dresslers syndrome is
difficult in asbestos-exposed patients who have undergone recent
cardiac surgery. Differentiation from mesothelioma or pleural
extension of a pulmonary malignancy is critical, and may be
difficult on clinical grounds (including positive gallium and positron emission scan). Pleural fluid cytology is useful for distinguishing benign from malignant effusions. It is not unusual for
nonspecific effusions to precede mesothelioma by several years.
If a malignancy has not manifested itself within 3 years, the
effusion is generally considered benign.
The diagnosis of chronic pleuritis manifested by pleuritic pain
is reached by excluding malignancies, because most other causes
of acute pleuritis do not result in chronic pain. Malignancy is
unlikely when pain persists for years with little or no clinical or
radiographic change.
Plaques: circumscribed pleural thickening. Pleural plaques are
indicators of exposure to asbestos. They are clearly the most
common manifestation of the inhalation, retention, and biologic
effect of asbestos. Their prevalence is most directly related to
duration from first exposure; they are rare within less than 20
years. Pleural plaques consistent with asbestos exposure appear
in chest films of 2.3% of U.S. males, a percentage that has been
703
Figure 10. Photomicrograph of H&E-stained section of lung

from a person with mild asbestosis. There is marked fibrosis of
the pleura with some subpleural fibrosis. Higher power magnification of the same section showed that minimal disease was
also present around the small respiratory bronchioles.
Figure 11. Photomicrograph of

H&E-stained section of a person with Grade III asbestosis
showing fibrosis in the lung parenchyma and overlying visceral pleura, with extension of
the fibrosis into the interlobular
septa.
704
Figure 12. Gross appearance at autopsy of asbestos-associated pleural

plaques overlying the lateral thoracic wall.
remarkably stable both for the general population in the early

1970s and veterans in the 1990s (94, 95).
Calcification is similarly related to duration. Smoking plays
no role in the prevalence of pleural plaques (68). Pleural plaques
are bilateral, but not symmetric, lesions of the parietal pleura.
Characteristically, they are found following the ribs on the lower
posterior thoracic wall (Figure 12) and over the central tendons
of the diaphragm (Figure 13). They are raised, sharply circumscribed with a smooth or with a rounded knobby surface, and
range in color from white to pale yellow. They generally spare
the costophrenic angles and apices of the thoracic cavity. Microscopically, they consist of mature collagen fibers arranged in
an open basket-weave pattern and are covered by flattened or
cuboidal mesothelial cells. They are relatively avascular and
acellular and show minimal inflammation. They are sharply demarcated from subpleural tissues and central calcification is common. Asbestos bodies are not seen in or adjacent to the lesions
(64). Isolated plaques may be associated with tuberculosis,
trauma, and hemothorax; however, multiple lesions having the
classic appearances described above are almost invariably associated with asbestos exposure.
The conventional chest film is a sensitive and appropriate
imaging method for plaques, although it may identify abnormalities that resemble plaques but are not. In the PA radiograph,
they are best seen in profile on the midlateral chest walls and
on the diaphragm or face on, and show serrated borders. HRCT
is not a practical screening method for demonstrating plaques
because of the separation between sections, the high radiation
exposure, and the lack of access to the test in some locations.
HRCT is useful to identify questionable abnormalities and to
resolve questions about structures that resemble plaques.
Typical pleural plaques are easily identified on plain films by
sharp, often foliate, borders (face on) and by a raised straight
surface with clear, cut-off edges when seen face on (Figures
1416) and as irregular margins (sometimes almost rectangular)
when seen in profile on the chest wall or diaphragm. Apparent
pleural thickening with gradually tapering or indistinct edges is
often due to subpleural fat or superimposed soft tissue; fat pads
below the parietal pleura typically occur in the midthoracic wall,
Figure 13. Gross appearance of large

asbestos-related pleural plaque over
the dome of the diaphragm.
Figure 14. En face (face on) pleural plaques in a chest film with minimal
parenchymal disease; worker was 54 years old at the time this chest
film was taken (1982) and was exposed to asbestos in the 1960s as an
insulation worker.
between the fourth and eighth ribs, as do pleural plaques (51).

Proper penetration is important on plain film; differentiation of
fat from pleural plaques may still be difficult but is readily made
by HRCT. Less typical plaques on the diaphragm may be difficult
to detect and should be distinguished from atelectatic streaks,
visceral folds, or diaphragmatic straightening caused by bullae.
Calcification is helpful but may not be apparent in an underpenetrated film (Figure 14). Axial CT scans often fail to image diaphragmatic plaques (96).
The origin of pleural plaques is not clear (97, 98). The burden
of asbestos fibers in lung tissue and of asbestos bodies in bronchoalveolar lavage fluid is greatly increased in patients with
diffuse pleural thickening or asbestosis and moderately increased
in patients with pleural plaques compared with unexposed subjects (99101). The presence of pleural plaques is correlated
with parenchymal disease, in particular fibrotic bands and both
peribronchiolar and alveolar fibrosis. However, peribronchiolar
fibrosis is absent in many cases with pleural plaques and present
in many cases without them (102).
Slow progression of plaques is typical. Approximately 85%
of heavily exposed workers showed pleural thickening (predominantly plaques) on plain film more than 40 years from first
exposure (103), as did up to 17% of environmentally exposed
populations (104). More than half the cases were bilateral.
The presence of plaques is associated with a greater risk of
mesothelioma and of lung cancer compared with subjects with
comparable histories of asbestos exposure who do not have
plaques (105, 106). This is thought to be due to greater exposure
or retained body burden, not malignant degeneration. Therefore,
the presence of pleural plaques should be interpreted as a marker
for elevated risk of malignancy, which may be higher than the
occupational history alone might suggest.
Although pleural plaques have long been considered inconse-
705
Figure 15. Pleural plaque, with linear calcification, seen on edge on the
right hemidiaphragm in a 72-year-old sheet metal worker. No visible
parenchymal disease.
quential markers of asbestos exposure, studies of large cohorts

have shown a significant reduction in lung function attributable
to the plaques, averaging about 5% of FVC, even when interstitial fibrosis (asbestosis) is absent radiographically (74, 76, 107).
The presence of circumscribed plaques can be associated with
restrictive impairment and diminished diffusing capacity on pulmonary function testing, even in the absence of radiographic
evidence of interstitial fibrosis (108, 109). Taking into account
the degree of interstitial fibrosis as measured by ILO profusion
score (described below), smoking, and duration of asbestos exposure, significant decrements in vital capacity have been observed:
a reduction of up 140 ml or more of FVC associated with circumscribed plaques (76). This has not been a consistent finding
(110, 111) and longitudinal studies have not shown a more rapid
decrement in pulmonary function in subjects with pleural
plaques (112). Decrements, when they occur, are probably related to early subclinical fibrosis. Dyspnea on exertion was reported more often among subjects with circumscribed pleural
thickening independent of parenchymal disease and appeared
to be proportional to the extent (110). There is a significant but
small association between the extent of circumscribed pleural
plaques and FVC, which is not seen with diffuse pleural thickening (112, 113). Even so, most people with pleural plaques
alone have well preserved lung function (55).
It is unclear whether this small effect on lung function is
sufficient to contribute to dyspnea but there is evidence that it
might. Half of subjects with pleural thickening but normal chest
films and normal lung function showed excessive ventilation
with exercise, which can contribute to dyspnea (114). Excessive
ventilation on exercise could be the result of decreased chest
wall and/or lung compliance caused by pleural thickening alone
or to decreased lung compliance and ventilationperfusion imbalance caused by parenchymal fibrosis that was not detected
radiographically.
Plaques are indicators of increased risk for the future development of asbestosis (94). This may reflect greater exposure or
retained body burden. An autopsy study has demonstrated more
frequent peribronchiolar fibrosis when plaques are present (90).
This finding, as well as derangements in gas exchange (114) and
evidence from HRCT, indicate that subradiographic asbestosis
may be present in some patients with only pleural plaques. The
presence of plaques is therefore an indication to monitor the
patient over time for interstitial fibrosis (115).
Diffuse pleural thickening. Diffuse thickening of the visceral
pleura is not sharply demarcated and is often associated with
fibrous strands (crows feet) extending into the parenchyma.
In large surveys of asbestos-exposed workers, diffuse pleural
thickening has ranged from 9 to 22% of those with pleural
disease. Both circumscribed and diffuse pleural thickening may
be present in the same hemithorax. Diffuse pleural thickening
superimposed on circumscribed plaques has been observed, often after pleural effusion (91).
The frequency of diffuse pleural thickening increases with
time from first exposure and is thought to be dose related (104).
Diffuse pleural thickening has been observed after acute pleuritis
(90). It may also be caused by extension of interstitial fibrosis
to the visceral pleura, consistent with the pleural migration of
asbestos fibers. The extent of diffuse pleural thickening seems
to be more or less uniformly distributed, the different degrees
being fairly equally often seen, however, in contradistinction to
circumscribed pleural thickening, in which the lowest categories
are more frequent (113). Lung burdens of asbestos in these
cases are intermediate between asbestosis and pleural plaques
(116118).
This condition affects the visceral pleural surface and is quite
different in appearance from the parietal pleural plaque. It consists of pale gray diffuse thickening that blends at the edges with
the more normal pleura. It may be extensive and cover a whole
lobe or whole lung and obliterate lobar fissures. It ranges in
thickness from less than 1 mm up to 1 cm or more. Adhesions to
the parietal pleura are common, particularly opposite to pleural
plaques. The lesion may show a gradient with immature granulation tissue and fibrin at the surface, progressing to mature collagen adjacent to the lung. The fibrosis may extend for a few
millimeters into the lung parenchyma and into the lobular septae.
The latter features do not constitute asbestosis.
Diffuse pleural thickening may have a significantly greater
impact on pulmonary function than circumscribed plaques. A
reduction of 270 ml of FVC has been associated with diffuse
pleural thickening (76, 119). Workers with diffuse pleural thickening have a significantly greater decrement in FVC (by a factor
of two or more) than those with circumscribed pleural thickening
(76, 113). This effect is unrelated to the radiographic extent of
pleural thickening; a similar reduction in FVC was seen with
little more than costophrenic angle blunting as with extensive
involvement (113). Decrements associated with diffuse pleural
thickening reflect pulmonary restriction as a result of adhesions
of the parietal with the visceral pleura. Restrictive impairment
is characteristic, with relative preservation of diffusing capacity
(pattern of entrapped lung).
707
Diffuse pleural fibrosis extends continuously over a portion

of the visceral pleura, often causing adhesions to the parietal
pleura, involving the fissures and obliterating the costophrenic
angle. The newly revised ILO classification (2003) recognizes
pleural thickening as diffuse only in the presence of and in
continuity with, an obliterated costophrenic angle (38). Localized subpleural parenchymal fibrosis is often present without
diffuse interstitial fibrosis (117). Calcification of the pleura occurs
with the passage of time, and may involve fissures. A rare variant
of visceral pleural fibrosis is progressive apical thickening associated with fibrosis of the upper lobe (120, 121).
Pachypleuritis is extensive, often bilateral, pleural fibrosis
with evidence of active inflammation histologically and by gallium uptake. Extension of fibrosis into the lung is often evident
radiographically as irregular pleural and pericardial borders, fibrous streaks, or crows feet and bands. Ventilatory failure
leading to CO2 retention, cor pulmonale, and death has been
described in four patients with bilateral involvement and little
or no parenchymal fibrosis, and in one patient with unilateral
pleural thickening. Decortication may be beneficial (122).
Rounded atelectasis. Rounded atelectasis (123, 124), also
known as shrinking pleuritis, contracted pleurisy, pleuroma, Blesovskys syndrome (125), or folded lung, presents radiographically as a mass and may be mistaken for a tumor (Figure 17).
The condition may result from pleuritis of any cause. The lesion
is thought to develop from infolding of thickened visceral pleura
with collapse of the intervening lung parenchyma. Clinical experience suggests that it is more likely to occur today as a result
of asbestos exposure than other causes. The classic comet sign
is pathognomonic and is often more readily seen on an HRCT
than on plain films. Clues to its identity are a band connecting the
mass to an area of thickened pleura and a slower evolution than
that of a lung cancer, so that previous films will show a similar
finding. Histologic examination shows folded and fibrotic visceral
pleura with atelectasis and variable amounts of chronic inflammation in the adjacent lung parenchyma. The sudden appearance
of rounded atelectasis may follow acute pleuritis with effusion.
Rounded atelectasis may be multiple and bilateral (124, 126).
Rounded atelectasis is important for the diagnostic pathologist to recognize as it is frequently removed surgically as a suspected peripheral lung cancer. Asbestos bodies and/or evidence
of asbestosis should be carefully sought.
Differential diagnosis, including rounded atelectasis and apical
thickening. Acute pleuritis of any cause can result in diffuse
pleural thickening that is indistinguishable from that associated
with asbestos, although such causes are usually unilateral. The
most likely causes, empyema, tuberculosis, and trauma, including
surgery, are likely to be identified in the medical history. Empyema in childhood or an infected pleural effusion associated with
pneumonia may not be.
The major differential diagnostic consideration with diffuse
pleural thickening is mesothelioma, which is progressive and
more likely to be symptomatic at the time of detection. On
occasion, when fibrosis and mesothelial proliferation are exuberant, the distinction is difficult clinically, radiographically, and
histologically. Apical thickening (120, 122) must also be distin-
Figure 16. Extensive evaluation in 1983 of a 65-year-old business executive who, in the 1950s, had worked in shipyards for approximately 2 years
and was exposed to high levels of asbestos. This case is unusual because both early asbestosis and a huge pleural plaque are unilateral. (A ) PA
film shows asbestosis and an extensive pleural plaque extending over three-quarters of the length of the hemothorax. Right costophrenic angle
is blunted but would not satisfy strict criteria for this according to the ILO classification. (B ) Lateral film, showing extensive calcified plaques over
diaphragm, also visible on left in PA film. (C ) Because of concern for possible mass in right lower lung lobe, PA film was repeated with nipple
markers: mass not seen in this view. (D ) Left anterior oblique, showing absence of other plaques on chest wall. (E ) Right anterior oblique, showing
detail of plaque. (F ) CT scan, showing plaque.
708
as part of the pathophysiologic process of asbestosis and

are not an independent entity.
Figure 17. Rounded atelectasis in a 57-year-old sheet metal worker. (A )

Presentation as a mass in the left chest. (B ) CT scan showing pleural
base and infolding of structures.
guished from mesothelioma and tuberculosis, which may be suggested by history and (previous) bacteriologic findings.
Chronic Airway Obstruction
Asbestos exposure has traditionally been considered to cause

predominantly restrictive physiologic abnormalities. The role of
asbestos as a cause of airway obstruction has been controversial.
However, asbestos exposure has long been known to be associated with an obstructive physiological abnormality (127129).
This association might arise in one or more of several ways:
Asbestos specifically causes obstructive abnormality.
Asbestos causes obstructive abnormality nonspecifically
(i.e., as do large burdens of most inorganic dusts) (83, 130).
Work leading to extensive asbestos exposure is frequently
associated with exposure to other agents affecting airways.
Confounding by tobacco smoking may lead to an association.
Anatomic and physiologic airway abnormalities develop
Asbestos-related chronic airway obstruction may result in

reduction in the FEV1/FVC ratio associated with reduced FEV1
(29, 76, 113, 127). Epidemiologic studies have demonstrated a
significant association between asbestos exposure or asbestosis
category as defined radiographically and reduction in FEV1,
FEV1/FVC ratio, and midexpiratory flow rates (111, 130133).
The relationship between surrogate measures of exposure and
the FEV1 and FEV1/FVC ratio also occurs in subjects who do
not have radiographic evidence of asbestosis (defined as an ILO
score exceeding 1/0) (130, 133, 134). A small effect has been
observed in lifelong nonsmokers (14, 113, 135, 136). This effect
begins in small airways, consistent with the known pathology of
bronchiolitis in early asbestosis (136, 137). Radiographically,
airflow abnormalities may also be associated with emphysema
(138).
Histologically, inflammation and airway fibrosis characterize
asbestos-related small airway disease. A major site of asbestos
deposition is in the walls of membranous and respiratory bronchioles. In the walls of membranous bronchioles this leads to
fibrosis and smooth muscle hyperplasia that are similar, but
more severe, than that produced by cigarette smoking (128, 139)
(Figures 4, 5, and 18). The respiratory bronchioles show fibrosis,
which extends into the alveolated portions of the walls and
alveolar ducts (Figure 19). In this regard, it differs from the lesion
of cigarette smoking, which primarily involves the nonalveolated
portions of the first generation of respiratory bronchioles (140).
Asbestos bodies are not present in the walls of the membranous
bronchioles, although inflammatory changes are present, but are
commonly seen in the walls of the respiratory bronchioles and/
or adjacent alveoli. Some authorities consider it appropriate to
describe these lesions as true asbestosis because the walls of
respiratory bronchioles are largely alveolated and therefore
within the gas exchange region of the lung (64). Others consider
the small airway lesions as distinct from asbestosis and refer to
the lesions of both membranous and respiratory bronchioles as
asbestos-induced small airway disease (12). These small airway
lesions are the likely anatomic basis for airflow limitation in
asbestos-exposed individuals.
In general, the magnitude of the asbestos effect on airway
function is relatively small. This effect, by itself, is unlikely to
result in functional impairment or the usual symptoms and signs
of chronic obstructive pulmonary disease. However, if superimposed on another disease process, the additional loss of function
due to the asbestos effect might contribute significantly to increased functional impairment, especially in persons with low
lung function.
Asbestos exposure independently contributes to accelerated
decline in airflow over time, whether or not exposure ceases (77,
129, 133, 134, 141). Dyspnea, cigarette smoking, diffuse pleural
thickening, honeycombing observed on HRCT scan, and indicators of active inflammation have been associated with worsening
obstruction (142). Effects on measures of early small airway
dysfunction (e.g., midexpiratory flow rates) in themselves are
unlikely to produce clinically relevant impairment, but may indicate an increased probability that disease will develop later (128,
129, 134, 143). Development or persistence of respiratory symptoms among asbestos-exposed workers is associated with accelerated loss of lung function, both FVC and FEV1 (30). In patients
with severe obstructive airway disease from another cause, the
additional contribution of asbestos-related airflow obstruction
might be functionally significant at low levels of lung function.
Short duration and low cumulative exposure are less likely to
produce significant obstructive abnormality (112, 134).
709
Figure 18. Photomicrograph of

asbestos-related smallairway disease, showing thickened membranous bronchiole. There is
also fibrosis around the airway,
and a mild chronic inflammatory cell infiltrate in its wall.
Assessment of functional impairment of clinical significance

(3) should generally be based on the restrictive findings associated with asbestosis, as these are more likely to be disabling.
However, the addition of obstructive disease adds to the level
of functional impairment (144). Treating restriction and obstruction separately may underestimate their combined effect on impairment. The normal indicator for restrictive impairment, total
lung capacity, has proven to be insensitive to total impairment
in subjects with both asbestosis and chronic obstructive lung
disease. In such cases, diffusing capacity and alveolararterial
oxygen difference may be more revealing (144). Some of the
restrictive component may be contributed by air trapping rather
than fibrosis (145).
Chronic obstructive airway disease that is not due to asbestos
(e.g., secondary to smoking) may complicate the recognition of
asbestosis. For example, total lung capacity may be normal when
both disorders are present, due to a restrictive process offsetting
air trapping (143). Whereas the FEV1/FVC ratio may be reduced
in asbestos-exposed persons with no or a low profusion of small,
irregular opacities, this ratio may also be normal in more advanced asbestosis (i.e., with higher profusion and diminished
FVC) because of a reduction in FVC (75).
Effects on airflow begin before the development of asbestosis
(129). In individuals who develop asbestosis, physiologic findings
associated with airflow obstruction (e.g., reduction in the FEV1/
FVC ratio) become less prominent as asbestosis progresses; this
may reflect increased pulmonary recoil.
The dose and time course of asbestos-associated airway abnormalities have received limited attention. Many available stud-
Figure 19. Photomicrograph of asbestos-related small airway disease,

in this case a respiratory bronchiole, with extension of the fibrosis into
the adjacent parenchyma (Grade II asbestosis; see Table 2).
710
TABLE 3. RECOMMENDATIONS FOR MANAGEMENT AFTER DIAGNOSIS OF ASBESTOSIS
1. Patient notification
1.1. Inform patient of work-related illness
1.2. Report to appropriate authority as occupational disease, as required by law
1.3. Inform patient that there are options for compensation
2. Impairment assessment
2.1. Conduct an assessment of functional impairment
2.2. Rate impairment in accordance with ATS criteria,* which are incorporated into the AMA Guides
3. Tertiary prevention
3.1. Smoking cessation (primary prevention for smoking-related disorders)
3.2. Withdrawal from further excessive exposure
3.3. Immunization (pneumococcal pneumonia, influenza)
3.4. Management of concurrent respiratory and other diseases
4. Monitoring
4.1. Chest film and pulmonary function testing should be conducted every 3 to 5 years
4.2. Active monitoring (periodic screening) for colon cancer
4.3. Observation and elevated index of suspicion but not screening for lung cancer, mesothelioma, gastrointestinal cancers
(other than colon)
5. Development of a patient-specific management plan for symptomatic disease
Definition of abbreviations: AMA American Medical Association; ATS American Thoracic Society.
* See Reference 3.
See Reference 157.
See text.
See References 4 and 5.
ies reflect relatively high historical levels of exposure. Among

nonsmoking Chinese asbestos workers, association of cumulative
exposure with functional effects was seen only among those with
long-term exposure (133).
Tobacco smoking is the predominant cause of chronic airway
obstruction in asbestos-exposed workers who smoke, although
occupational exposures can be significant. The association between airway obstruction and exposure to asbestos has been well
demonstrated in nonsmokers, and in some studies the association
between exposure and airway obstruction is seen only among
nonsmokers (131); among smoking asbestos-exposed workers,
smoking accounts for most of the small airway abnormality (111,
127, 135, 141, 142). In addition to smoking, other occupational
exposures might contribute to chronic obstructive airway disease; effects of asbestos in producing airflow obstruction are
likely to be additive to these. There may be an interaction between smoking and asbestos in the development of airway obstruction, as has been demonstrated in animal models (146), but
this has not yet been demonstrated for human subjects.
IMPLICATIONS OF DIAGNOSIS FOR

PATIENT MANAGEMENT
A history of significant asbestos exposure obligates the responsible physician to provide a management plan for the patient that
takes into consideration current disease and impairment as well
as future risk (147). A recommended management plan is summarized in Table 3.
Workers referred for evaluation of asbestos-related disease
today differ from those referred in past years. Exposure to asbestos among these workers is likely to be more remote in time
and to have been less intense. Exposed workers may live longer
and progress later to more advanced stages of disease. They are
more likely to survive to develop additional outcomes associated
with asbestos, such as malignancy, and to present more complicated management challenges (148).
Actions Required before Disease Is Apparent
A recent or short-term history of exposure to asbestos, particularly in the absence of detail on duration and intensity, requires
the clinician at a minimum to educate the patient with respect
to latency, the exposureresponse relationship characteristic of

asbestos-related diseases, and the future risk of malignant disease. Reassurance should be offered where appropriate and the
risk placed into the context of the exposure history. This is often
an excellent opportunity at the same time to review the patients
history, work hygiene practices, behavior and attitudes toward
cigarette smoking, as well as exposure to other occupational and
environmental carcinogens (149).
For all patients presenting with a history of significant or
possibly significant exposure, at a minimum a baseline, highquality chest film should be obtained, together with spirometry
and a single-breath diffusing capacity that conform to American
Thoracic Society guidelines. Complete pulmonary function testing should be obtained if clinically indicated. Workers who have
had exposure to asbestos have also often worked in other dusty
occupations. They and their families may have lived in communities where they experienced environmental exposures.
The sensitivity of the plain chest film for identifying asbestosis
at a profusion level of 1/0 (in the ILO classification system) has
been estimated at or slightly below 90%. The corresponding
specificity has been estimated at 93%. Applied to populations
with varying prevalence of disease, the positive predictive value
of the minimally abnormal chest film alone in making the diagnosis of asbestosis may fall below 30% when exposure to asbestos
has been infrequent and exceed 50% when it has been prevalent.
This suggests that screening programs based on the chest film
alone may vary considerably in their yield of true cases depending on the characteristics of the population being screened.
In the general population and for occupational groups with low
levels of exposure they may be unreliable in identifying asbestosis. The application of multiple criteria, as outlined in this statement, is a preferable approach (150). However, combinations
of tests for a specific criterion, such as a hypothetical requirement
that multiple tests for pulmonary function be abnormal, would
reduce the sensitivity without enhancing specificity for asbestosrelated disease; in general, the most sensitive test for a particular
criterion is preferable (2).
Persons identified as having asbestos-related disease or a
significant exposure history should be informed of the risk of
progression of disease, the risk of malignancy, and especially
the interaction between smoking and asbestos exposure in enhancing the risk of lung cancer. Such persons who smoke may
be more motivated to consider cessation when the connection
between asbestos and the risk of respiratory impairment and of
malignancy is brought up at this time (151). The risk conferred
by other occupational and environmental carcinogens should
also be emphasized at this time.
The question of monitoring for asbestos-related disease is
complicated by requirements for occupational surveillance, especially for those with minimal exposure. The Occupational Safety
and Health Administration asbestos standard requires employers to monitor their asbestos-exposed workers during employment but makes no provision beyond the period of employment,
despite the latency, and private insurance may or may not allow
the expense thereafter (8).
Persons with a history of exposure to asbestos but no manifest
disease, and for whom the time since initial exposure is 10 years
or more, may reasonably be monitored with chest films and
pulmonary function studies every 3 to 5 years to identify the
onset of asbestos-related disease.
Persons with a history of exposure to asbestos are also at risk
for asbestos-related malignancies. Periodic health surveillance
for lung cancer or mesothelioma is not recommended. Screening
for lung cancer using periodic (annual) chest films, low-dose
computed tomography, or sputum cytology has not been shown
to be effective in preventing mortality or improving quality of life
in populations of smokers without known adverse occupational
exposures (152, 153). New technologies (e.g., low-dose spiral CT
scanning) are being evaluated for use in high-risk groups (153).
The risk of extrathoracic malignancies may also be increased in
asbestos-exposed workers. Studies suggest that there may be an
elevation in the risk of colon cancer (149, 150), although this
remains controversial (154). Because colon cancer is often treatable and screening for colorectal cancer is recommended by the
American Cancer Society for persons more than 50 years of age
(155), it is reasonable on the basis of current evidence to screen
for this condition. The risk of cancer of the larynx (156) and
possibly gastrointestinal cancers other than colon, including pancreas, stomach, and esophagus (154), may also be increased with
asbestos exposure, but the presence and magnitude of an association with asbestos remain controversial for extrathoracic cancers
(154). Routine screening for these cancers is in any case not practical
at present.
No prophylactic medication or treatment is currently available to prevent the development or progression of asbestosis or
other asbestos-related diseases, once exposure has occurred.
Actions Required after Diagnosis
The diagnosis of asbestosis, in particular, imposes a duty to

inform the patient that he or she has a disease that is workrelated, to report the disease, and to inform the patient that he
or she may have legal or adjudication options for compensation.
The role of the physician in this compensation process includes
performing an objective evaluation of impairment consistent
with the rules of the specific compensation system. Guidelines
developed by the American Thoracic Society (3) may be of use
and are incorporated into the AMA Guides to the Evaluation
of Permanent Impairment (157). As in the management of any
lung disorder, the physician should also manage the clinical manifestations of the disease and counsel the patient to protect remaining lung function.
The patient with evidence of asbestosis should be considered
to be at risk of progressive lung disease, whatever the level of
impairment on first encounter. It seems logical that removal
from further exposure to asbestos or other significant occupational and environmental exposures may avoid more rapid pro-
711
gression of lung disease, although specific evidence for this is

lacking. However, if such exposures are minimal and are well
within occupational guidelines, care must be taken not to deprive
the patient of a livelihood for no clinical benefit.
Immunization against pneumococcal pneumonia and annual
influenza vaccine should be administered unless contraindicated
for other reasons. Effective management of concurrent chronic
obstructive pulmonary disease or asthma, if present, may reduce
morbidity from mixed disease.
Severe asbestosis is rare in the United States and other countries with generally effective occupational health regulation. Cor
pulmonale, secondary polycythemia, and respiratory insufficiency
and failure are all treated in the conventional manner in patients
with asbestosis.
In the spring of 2000, the Association of Occupational and
Environmental Clinics adopted a resolution recommending necessary standards for screening programs (158). This action was
taken in response to the proliferation of screening programs
undertaken to identify cases for possible legal actions in which
counseling and education may be lacking (159), but the recommendations also apply to those conducted for patient care and
protection. Their recommendations were consistent with those
given above and also emphasized timely physician disclosure of
results to the patient, appropriate medical follow-up, and patient
education. The National Institute of Occupational Safety and
Health has outlined elements of an adequate screening program,
with special reference to screening for asbestos-related disorders
in currently employed mineworkers, in a white paper produced
in 2002 that has received little attention (160). The National
Institute for Occupational Safety and Health recommended that
such programs should be under the direction of a qualified
physician or other qualified health care provider knowledgeable
in the field and competent to administer it, and documented
with written reports to workers and employers (the latter provision that would not necessarily be applicable to workers who
had separated from the employer). However, the National Institute for Occupational Safety and Health did not address the
issue of counseling in that document or clinical interventions to
reduce future risk.
CONCLUSIONS
The diagnosis of nonmalignant asbestos-related disease rests, as
it did in 1986, on the essential criteria described: a compatible
structural lesion, evidence of exposure, and exclusion of other
plausible conditions, with an additional requirement for impairment assessment if the other three criteria suggest asbestosrelated disease (2). Each criterion may be satisfied by one of a
number of findings or tests. The 2004 criteria are open to future
testing modalities if and when they are validated. For example,
HRCT has greatly increased the sensitivity of detection and has
become a standard method of imaging. Evidence for exposure
still rests on the occupational history, the demonstration of asbestos fibers or bodies, or pleural plaques. Impairment evaluation
is largely unchanged from 1986 and remains an essential part of
the clinical assessment. Potentially confounding conditions, such
as idiopathic pulmonary fibrosis, are better understood and many,
such as tuberculosis, are less common than in the past so that
the clinical picture is less often confusing.
These criteria and the guidelines that support them are compatible with the Helsinki criteria, developed by an expert group
in 1997, which represents substantial consensus worldwide (147).
The guidelines supporting these criteria will undoubtedly change
again in future, but the present guidelines should provide a
reliable basis for clinical diagnosis for some years to come.
712
This statement was developed by an ad hoc subcommittee of the

Scientific Assembly on Environmental and Occupational Health of
the American Thoracic Society. Members of the committee are as
follows:
TEE L. GUIDOTTI, M.D., M.P.H., Chair
George Washington University Medical Center, Washington, DC
ALBERT MILLER, M.D.
St. Vincent Catholic Medical Center of New York, Brooklyn-Queens
Service Region, Jamaica, NY
DAVID CHRISTIANI, M.D., M.P.H.
Harvard School of Public Health, Boston, MA
GREGORY WAGNER, M.D.
National Institute for Occupational Safety and Health,
Morgantown, WV
JOHN BALMES, M.D.
University of California San Francisco, San Francisco, CA
PHILIP HARBER, M.D., M.P.H.
University of California Los Angeles, Los Angeles, CA
CARL ANDREW BRODKIN, M.D., M.P.H.
University of Washington, Seattle, WA
WILLIAM ROM, M.D., M.P.H.
New York University School of Medicine, New York, NY
GUNNAR HILLERDAL, M.D.
Karolinska Institute, Stockholm, Sweden
MICHAEL HARBUT, M.D., M.P.H.
Center for Occupational and Environmental Medicine,
Royal Oak, MI
FRANCIS H. Y. GREEN, M.D.
University of Calgary, Calgary, AB, Canada
Acknowledgment : The statement subcommittee thanks the following for contributions, assistance, and suggestions: William Beckett, M.D., M.P.H. (University
of Rochester, Rochester, NY) and Jerrold L. Abraham, M.D. (State University
of New York, Syracuse, NY). Gross histology and photomicrographs were supplied
by Francis H. Y. Green, M.D. Radiographs were supplied by Tee L. Guidotti,
M.D., M.P.H.
References
1. Committee on Nonoccupational Health Risks of Asbestiform Fibers,
Board of Toxicology and Environmental Health Hazards, National
Research Council. Asbestiform fibers: nonoccupational health risks.
Washington DC: National Academies Press; 1984. p. 2429.
2. American Thoracic Society. The diagnosis of nonmalignant diseases
related to asbestos. Am Rev Respir Dis 1986;134:363368.
3. American Thoracic Society Ad Hoc Committee on Impairment/Disability Criteria. Evaluation of impairment/disability secondary to respiratory disorders. Am Rev Respir Dis 1986;134:12051209.
4. American Thoracic Society. Lung function testing: selection of reference
values and interpretive strategies. Am Rev Respir Dis 1991;144:1202
1218.
5. Ferris B. Epidemiology standardization project. Am Rev Respir Dis
1978;118:1113.
6. Virta RL. Some facts about asbestos. Fact sheet FS-01201. Reston,
VA: U.S. Geologic Survey, U.S. Department of Interior. Available
online at http://pubs.usgs.gov/factsheet/fs012-01/. Accessed July 29,
2004.
7. U.S. Environmental Protection Agency. Region 8 Superfund, Libby.
www.epa.gov/region8/superfund/libby/. Accessed July 29, 2004.
8. U.S. Department of Labor, Occupational Safety and Health Administration. Safety and health topics: asbestos. Available online at http://
www.osha.gov/SLTC/asbestos. Accessed July 29, 2004.
9. Churg A, Wright JL, Depaoli L, Wiggs B. Mineralogic correlates of
fibrosis in chrysotile miners and millers. Am Rev Respir Dis 1989;
139:891896.
10. Churg A, Wright J, Wiggs B, DePaoli L. Mineralogic parameters related
to amosite asbestos-induced fibrosis in humans. Am Rev Respir Dis
1990;142:13311336.
11. Rom WV. Asbestos-related diseases. In: Environmental and occupational medicine, 3rd ed. Philadelphia, PA: Lippincott-Raven; 1998.
p. 349375.
12. Rom WN, Bitterman PB, Rennard SI, Cantin AC, Crystal RG. Characterization of the lower respiratory tract inflammation of non-smoking
individuals with interstitual lung disease associated with the chronic
inhalation of inorganic dusts. Am Rev Respir Dis 1987;137:14291434.
13. Rom WN, Travis WD, Brody AR. Cellular and molecular basis of
the asbestos-related diseases [State of the Art]. Am Rev Respir Dis
1991;143:408422.
14. Wright JL, Cagle P, Churg A, Colby TV, Myers J. Diseases of the small
airways. Am Rev Respir Dis 1992;146:240262.
15. Jaurand MC, Gaudichet A, Atassi K, Sebastien P, Bignon J. Relationship between the number of asbestos fibres and the cellular and
enzymatic content of bronchoalveolar fluid in asbestos exposed subjects. Bull Eur Physiopathol Respir 1980;16:595606.
16. Begin R, Cantin A, Berthiaume Y, Boileau R, Peloquin S, Masse S.
Airway function in lifetime-nonsmoking older asbestos workers. Am
J Med 1983;75:631638.
17. Churg A, Wright JL. Small-airway lesions in patients exposed to nonasbestos mineral dusts. Hum Pathol 1983;14:688693.
18. Dai J, Gilks B, Price K, Churg A. Mineral dusts directly induce epithelial
and interstitial fibrogenic mediators and matrix components in the
airway wall. Am J Respir Crit Care Med 1998;158:19071913.
19. De Vuyst P, Karjalainen A, Dumortier P, Pairon J-C, Monso E, Brochard P, Teschler H, Tossavainen A, Gibbs A. Guidelines for mineral
fibre analyses in biological samples: report of the ERS Working
Group. Eur Respir J 1998;11:14161426.
20. Churg A. Fiber counting and analysis in the diagnosis of asbestos-related
disease. Hum Pathol 1982;13:381392.
21. Roggli VL, Coin PG, MacIntyre NR, Bell DY. Asbestos content of
bronchoalveolar lavage fluid: a comparison of light and scanning
electron microscopic analysis. Acta Cytol 1994;38:502510.
22. Johnson NF, Haslam PL, Dewar A, Newman-Taylor AJ, Turner-Warwick M. Identification of inorganic dust particles in bronchoalveolar
lavage macrophages by energy dispersive x-ray microanalysis. Arch
Environ Health 1986;41:133144.
23. Morgan A, Holmes A. Concentrations and characteristics of amphibole
fibres in the lungs of workers exposed to crocidolite in the British
gas-mask factories, and elsewhere, during the Second World War. Br
J Ind Med 1982;39:6269.
24. Schwartz DA, Galvin JR, Burmeister LF, Merchant RK, Dayton CS,
Merchant JA, Hunninghake GW. The clinical utility and reliability
of asbestos bodies in bronchoalveolar fluid. Am Rev Respir Dis 1991;
144:684688.
25. Churg A, Warnock ML. Analysis of the cores of asbestos bodies from
members of the general population: patients with probable lowdegree exposure to asbestos. Am Rev Respir Dis 1979;120:781786.
26. Dodson RF, Williams MG, Corn CJ, Brollo A, Bianchi C. Asbestos
content of lung tissue, lymph nodes, and pleural plaques from former
shipyard workers. Am Rev Respir Dis 1990;142:843847.
27. Xaubet A, Rodriguez-Roisin R, Bombi JA, Marin A, Roca J, AgustiVidal A. Correlation of bronchoalveolar lavage and clinical and functional findings in asbestosis. Am Rev Respir Dis 1986;133:848854.
28. Vathesatogkit P, Harkin TJ, Addrizzo-Harris DJ, Bodkin M, Crane M,
Rom WN. Clinical correlation of asbestos bodies in bronchoalveolar
lavage fluid [abstract]. Am J Respir Crit Care Med 2003;167:A684.
29. Brodkin CA, Barnhart S, Anderson G, Checkoway H, Omenn GS,
Rosenstock L. Correlation between respiratory symptoms and pulmonary function in asbestos-exposed workers. Am Rev Respir Dis 1993;
148:3237.
30. Brodkin CA, Barnhart S, Checkoway H, Balmes J, Omenn GS, Rosenstock L. Longitudinal pattern of reported symptoms and accelerated
ventilatory loss in asbestos-exposed workers. Chest 1996;109:120126.
31. Yates DH, Browne K, Stidolph PN, Neville E. Asbestos-related bilateral
diffuse pleural thickening: natural history of radiographic and lung
function abnormalities. Am J Respir Crit Care Med 1996;153:301306.
32. Committee on Occupational and Environmental Health of the American Lung Association of San Diego and Imperial Counties. Taking
the occupational history. Ann Intern Med l983;99:641651.
33. Welch LS, Michaels D, Zoloth SR. The national sheet metal worker
asbestos disease screening program: radiologic findings. Am J Ind
Med 1994;25:635648.
34. Epler GR, Gerald MX, Gaensler EA, Carrington CB. Asbestos-related
disease from household exposure. Respiration (Herrlisheim) 1980;39:
229240.
35. Weill H, Waggenspack C, Bailey W, Ziskin M, Rossiter C. Radiographic
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
and physiologic patterns among workers engaged in manufacture of

asbestos cement products. J Occup Med 1973;15:248252.
Markowitz SB, Marabia A, Lilis R, Miller A, Nicholson WJ, Levin S.
Clinical predictors of mortality from asbestosis in the North American
Insulator Cohort, 19811991. Am J Respir Crit Care Med 1997;156:
101108.
Murphy RL Jr, Gaensler EA, Holford SK, Del Bono EA, Epler G.
Crackles in the early detection of asbestosis. Am Rev Respir Dis 1984;
129:375379.
International Labour Office. International classification of radiographs
of pneumoconioses. Geneva, Switzerland: International Labour Organization; 2003.
Harkin TJ, McGuinness G, Goldring R, Parker JE, Crane M, Naidich
DP. Differentiation of the ILO boundary chest roentgenograph (0/1
to 1/0) in asbestosis by high-resolution computed tomography scan,
alveolitis, and respiratory impairment. J Occup Environ Med 1996;
38:4652.
Kipen HM, Lilis R, Suzuki Y, Valciukas JA, Selikoff IJ. Pulmonary
fibrosis in asbestos insulation workers with lung cancer: a radiological
and histopathological evaluation. Br J Ind Med 1987;44:96100.
Epler GR, McLoud TC, Gaensler EA, Mikus JP, Carrington CB. Normal chest roentgenograms in chronic diffuse infiltrative lung disease.
N Engl J Med 1978;298:934939.
Aberle DR, Gamsu G, Ray CS. High-resolution CT of benign asbestosrelated diseases: clinical and radiographic correlation. Am J Roentgenol 1988;151:883891.
Schwartz DA, Galvin JR, Yagla SJ, Speakman SB, Merchant JA, Hunninghake GW. Restrictive lung function and asbestos-induced pleural
fibrosis: a quantitative approach. J Clin Invest 1993;91:26852692.
Lee YC, Runnion CK, Pang SC, de Klerk NH, Musk AW. Increased
body mass index is related to apparent circumscribed pleural thickening on plain chest radiographs. Am J Ind Med 2001;39:112116.
Ameille J, Brochard, Brechot JM, Pascano T, Cherin A, Raix A, Fredy
M, Bignon J. Pleural thickening: a comparison of oblique chest radiographs and high-resolution computed tomography in subjects exposed
to low levels of asbestos pollution. Int Arch Occup Environ Health
1993;64:545548.
Genevois PA, De Vuyst P, Dedeire S, Cosaert J, Vande Weyer R,
Sturyven J. Conventional and high-resolution CT in asymptomatic
asbestos-exposed workers. Acta Radiol 1994;35:226229.
Genevois PA, de Maertaeler V, Madani A, Winant C, Sergent G, De
Vuyst P. Asbestosis, pleural plaques and diffuse pleural thickening:
three distinct benign responses to asbestos exposure. Eur Respir J 1998;
11:10211027.
Neri S, Borashi P, Antonelli A, Falaschi F, Baschieri L. Pulmonary
function, smoking habits, and high resolution computed tomography
(HRCT) early abnormality of lung and pleural fibrosis in shipyard
workers exposed to asbestos. Am J Ind Med 1996;30:588595.
Gamsu G, Salmon CJ, Warnock ML, Blanc PD. CT quantification of
interstitial fibrosis in patients who have asbestosis: a comparison of
two methods. AJR Am J Roentgenol 1995;164:6368.
Staples CA, Gamsu G, Ray CS, Webb WR. High resolution computed
tomography and lung function in asbestos-exposed workers with normal chest radiographs. Am Rev Respir Dis 1989;139:15021508.
Sargent EN, Boswell WD Jr, Ralls PW, Markovitz A. Subpleural fat
pads in patients exposed to asbestos: distinction from non-calcified
pleural plaques. Radiology 1984;152:273277.
Staples CA. Computed tomography in the evaluation of benign asbestosrelated disorders. Radiol Clin North Am 1992;30:11911207.
Webb WR, Muller NL, Naidich DP. High-resolution CT of the lung,
3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001. Chapter
4, Diseases characterized primarily by linear and reticular opacities.
p. 236251.
Kraus T, Raithel HJ, Lehnert G. Computer-assisted classification system
for chest X-ray and computed tomography findings in occupational
lung disease. Int Arch Occup Environ Health 1997;69:482486.
Van Cleemput J, De Raeve H, Verschakelen JA, Rombouts J, Lacquet
LM, Nemery B. Surface of localized pleural plaques quantitated by
computed tomography scanning: no relation with cumulative asbestos
exposure and no effect on lung function. Am J Respir Crit Care Med
2001;163:705710.
De Vuyst P, Jedwab J, Dumortier P, Vandermoten G, Vande Weyer
R, Yernault JC. Asbestos bodies in bronchoalveolar lavage. Am Rev
Respir Dis 1982;126:972976.
De Vuyst P, Dumortier P, Moulin E, Yourassowsky N, Roomans P, de
Francquen P, Yernault JC. Asbestos bodies in bronchoalveolar lavage
reflect lung asbestos body concentration. Eur Respir J 1988;1:362367.
713
58. Karjalainen A, Antilla S, Mantyla T, Taskinen E, Kyyronen P, Tukiainen
P. Asbestos bodies in bronchoalveolar lavage fluid in relation to
occupational history. Am J Ind Med 1994;26:645654.
59. De Vuyst P, Dumortier P, Moulin E, Yourassowsky N, Yernault JC.
Diagnostic value of asbestos bodies in bronchoalveolar lavage fluid.
Am Rev Respir Dis 1987;136:12191224.
60. Rom WN, Churg A, Leapman R, Fiori C, Swyt C. Evaluation of alveolar
macrophage particle burden in individuals occupationally exposed to
inorganic dusts. J Aerosol Med 1990;3:S43S56.
61. Sartorelli P, Scancarello G, Romeo R, Marciano` G, Rottoli P, Arcangeli
G, Palmi S. Asbestos exposure assessment by mineralogical analysis of
bronchoalveolar lavage fluid. J Occup Environ Med 2001;43:872881.
62. Sebastien P, Armstrong B, Monchaux G, Bignon J. Asbestos bodies in
bronchoalveolar lavage fluid and in lung parenchyma. Am Rev Respir
Dis 1988;137:7578.
63. Teschler H, Heinz-Friedrichs K, Hoheisel GR, Wick G, Soltner U,
Thompson AB, Konietzko N, Costabel U. Asbestos fibers in bronchoalveolar lavage and lung tissue of former asbestos workers. Am
J Respir Crit Care Med 1994;149:641645.
64. Craighead JE, Abraham JL, Churg A, Green FHY, Kleinerman J, Pratt
PC, Seemayer TA, Vallyathan V, Weill H. The pathology of asbestosassociated diseases of the lungs and pleural cavities: diagnostic criteria
and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pathologists and the National
Institute for Occupational Safety and Health. Arch Pathol Lab Med
1982;106:543596.
65. Green FH, Attfield M. Pathology standards for asbestosis. Scand J Work
Environ Health 1983;9:162168.
66. Green FHY, Harley R, Vallyathan V, Althouse R, Fick G, Dement J,
Mitha R, Pooley F. Exposure and mineralogic correlates of pulmonary
fibrosis in chrysotile asbestos workers. Occup Environ Med 1997;54:
549559.
67. Barnhart S, Thornquist M, Omenn GS, Goodman G, Feigl P, Rosenstock L. The degree of roentgenographic parenchymal opacities attributable to smoking among asbestos-exposed subjects. Am Rev Respir
Med 1990;141:11021106.
68. Zitting AJ, Karjalainen A, Impivaara O, Kuusela T, Maki J, Tossavainen
A, Jarvisalo J. Radiographic small lung opacities and pleural abnormalities in relation to smoking, urbanization status and occupational
asbestos exposure in Finland. J Occup Environ Med 1996;38:602609.
69. Lilis R, Selikoff IJ, Lerman Y, Seidman H, Gelb SK. Asbestosis: interstitial pulmonary fibrosis and pleural fibrosis in a cohort of asbestos
insulation workers: influence of cigarette smoking. Am J Ind Med 1986;
10:459470.
70. Ehrlich R, Lilis R, Chan E, Nicholson WJ, Selikoff IJ. Long-term radiological effects of short-term exposure to amosite among factory workers. Br J Ind Med 1992;49:268275.
71. Green RA, Dimcheff DG. Massive bilateral upper lobe fibrosis secondary to asbestos exposure. Chest 1974;65:5255.
72. Hillerdal G. Pleural and parenchymal fibrosis mainly affecting the upper
lung in persons exposed to asbestos. Respir Med 1990;84:129134.
73. Morgan A, Holmes A. Distribution and characteristics of amphibole
asbestos fibres, measured with the light microscope, in the left lung
of an insulation worker. Br J Ind Med 1983;40:4550.
74. Miller A, Lilis R, Godbold J, Chan E, Selikoff IJ. Relationship of
pulmonary function to radiographic interstitial fibrosis in 2,611 longterm asbestos insulators: an assessment of the International Labour
Office profusion score. Am Rev Respir Dis 1992;145:263270.
75. Selikoff IJ, Churg J, Hammond EC. Asbestos exposure and neoplasia.
JAMA 1964;188:2226.
76. Schwartz DA, Fuortes LJ, Galvin JR, Burmeister LF, Schmidt LE,
Leistikow BN, LaMarte FP, Merchant JA. Asbestos-induced pleural
fibrosis and impaired lung function. Am Rev Respir Dis 1990;141:321
326.
77. Rom WN. Accelerated loss of lung function and alveolitis in a longitudinal study of non-smoking individuals with occupational exposure to
asbestos. Am J Ind Med 1992;21:835844.
78. Becklake M, Case B. Fiber burden and asbestos-related lung disease:
determinants of doseresponse relationships. Am J Respir Crit Care
Med 1994;150:14881492.
79. Roggli VL, Pratt PC. Numbers of asbestos bodies on iron-stained sections in relation to asbestos body counts in lung tissue digests. Hum
Pathol 1983;14:355361.
80. Dodson RF, Williams MG Jr, OSullivan MF, Corn CJ, Greenberg
SD, Hurst GA. A comparison of the ferruginous and uncoated fiber
content in the lungs of former asbestos workers. Am Rev Respir Dis
1985;132:143147.
714
81. Seal RME. Current views on pathological aspects of asbestosis: the

unresolved questions and problems. In: Wagner JC, editor. Biological
effects of mineral fibers. Lyon, France: International Agency for
Research on Cancer; 1980. p. 217235.
82. Miller A, Langer AM, Tierstein AS, Selikoff IJ. Nonspecific interstitial pulmonary fibrosis: association with asbestos fibers detected by
electron microscopy. N Engl J Med 1975;292:9194.
83. Hnizdo E, Sullivan P, Bang KM, Wagner GR. Association between
chronic obstructive pulmonary disease and employment by industry
and occupational in the US population: a study of data from the
Third National Health and Nutrition Examination Survey. Am J
Epidemiol 2002;156:738746.
84. Hammar SP, Hallman KO. Localized inflammatory pulmonary disease
in subjects occupationally exposed to asbestos. Chest 1993;103:1792
1799.
85. Al-Jarad N, Wilkinson P, Pearson MC, Rudd RM. A new high resolution
computed tomography scoring system for pulmonary fibrosis, pleural
disease, and emphysema in patients who have asbestos related disease. Br J Ind Med 1992;49:7384.
86. Webb WR, Cooper C, Gamsu G. Interlobar pleural plaque mimicking
a lung nodule in a patient with asbestos exposure. J Comput Assist
Tomogr 1983;7:135136.
87. Hillerdal G, Ozesmi M. Benign asbestos pleural effusion: 73 exudates
in 60 patients. Eur J Respir Dis 1987;71:113121.
88. Epler GR, Gaensler EA. Prevalence of asbestos pleural effusion in a
working population. JAMA 1982;247:617622.
89. Robinson BWS, Musk AW. Benign asbestos pleural effusion: diagnosis
and course. Thorax 1981;36:896900.
90. Lilis R, Lerman Y, Selikoff IJ. Symptomatic benign pleural effusions
among asbestos insulation workers: residual radiographic abnormalities. Br J Ind Med 1988;45:443449.
91. Miller A, Miller JA. Diffuse pleural thickening superimposed on circumscribed pleural thickening related to asbestos exposure. Am J Ind
Med 1993;23:859871.
92. Miller A. Chronic pleuritic pain in four patients with asbestos induced
pleural fibrosis. Br J Ind Med 1990;47:147153.
93. Fielding DI, McKeon JL, Oliver WA, Matar K, Brown IG. Pleurectomy
for persistent pain in benign asbestos-related disease. Thorax 1995;50:
181183.
94. Rogan WJ, Gladen BC, Ragan NB, Anderson HA. US prevalence of
occupational pleural thickening: a look at x-rays from the First National Health and Nutrition Examination Survey. Am J Epidemiol
1987;126:893900.
95. Miller JA, Zurlo JV. Asbestos plaques in a typical veterans hospital
population. Am J Ind Med 1996;30:726729.
96. Begin R, Boctor M, Bergeron D, Cantin A, Berthiaume Y, Peloquin
S, Bisson G, Lamoureux G. Radiographic assessment of pleuropulmonary disease in asbestos workers: posteroanterior, four view films, and
computed tomograms of the thorax. Br J Ind Med 1984;41:373383.
97. Churg A. The pathogenesis of pleural plaques. Indoor Built Environ
1997;6:7378.
98. Taskinen E, Ahlmon K, Wiikeri M. A current hypothesis of the lymphatic transport of inspired dust to the parietal pleura. Chest 1973;64:
193196.
99. Churg A, Vedal S. Fiber burden and patterns of asbestos-related disease
in workers with heavy mixed amosite and chrysotile exposure. Am J
Respir Crit Care Med 1994;150:663669.
100. Churg A, Wright JL, Vedal S. Fiber burden and patterns of asbestosrelated disease chrysotile miners and millers. Am Rev Respir Dis
1993;148:2531.
101. Kishimoto T, Ono T, Okada K, Ito H. Relationship between number
of asbestos bodies in autopsy lung and pleural plaques on chest x-ray
film. Chest 1989;95:549552.
102. Sison RF, Hruban RH, Moore GW, Kuhlman JE, Wheeler PS, Hutchins
GM. Pulmonary disease associated with pleural asbestos plaques.
Chest 1989;95:831835.
103. Lilis R, Miller A, Godbold J, Chan E, Selikoff IJ. Radiographic abnormalities in asbestos insulators: effects of duration from onset of exposure and smoking; relationships of dyspnea with parenchymal and
pleural fibrosis. Am J Ind Med 1991;20:115.
104. Schwartz DA. New developments in asbestos-induced pleural disease.
Chest 1991;99:191198.
105. Hillerdal G, Henderson DW. Asbestos, asbestosis, pleural plaques and
lung cancer. Scand J Work Environ Health 1997;23:93103.
106. Hillerdal G. Pleural plaques and the risk for bronchial carcinoma and
mesothelioma. Chest 1994;105:144150.
107. Jarvolm B, Sanden A. Pleural plaques and respiratory function. Am J

Ind Med 1986;10:419426.
108. Hjortsberg U, rbaek P, Aborelius M Jr, Ranstam J, Welinder H.
Railroad workers with pleural plaques. I. Spirometric and nitrogen
washout investigation on smoking and nonsmoking asbestos-exposed
workers. Am J Ind Med 1988;14:635641.
109. Oliver LC, Eisen EA, Greene R, Sprince NL. Asbestos-related pleural
plaques and lung function. Am J Ind Med 1988;14:649656.
110. Bourbeau J, Ernst P, Chrome J, Armstrong B, Becklake MR. The
relationship between respiratory impairment and asbestos-related
pleural abnormality in an active work force. Am Rev Respir Dis
1990;142:837842.
111. Ohlson G, Rydman T, Sundell L, Bodin L, Hogstedt C. Decreased
lung function in long-term asbestos cement workers: a cross-sectional
study. Am J Ind Med 1984;5:359366.
112. Lilis R, Miller A, Godbold J, Chan E, Selikoff IJ. Pulmonary function
and pleural fibrosis: quantitative relationships with an integrative
index of pleural abnormalities. Am J Ind Med 1991;29:145161.
113. Ohlson C-G, Bodin L, Rydman T, Hogstedt C. Ventilatory decrements
in former asbestos cement workers: a four year follow up. Br J Ind
Med 1985;42:612616.
114. Miller A, Bhuptani A, Sloane MF, Brown LK, Teirstein AS. Cardiorespiratory responses to incremental exercise in patients with asbestosrelated pleural thickening and normal or slightly abnormal lung function. Chest 1993;103:10451050.
115. Hillerdal G. Non-malignant asbestos pleural disease. Thorax 1981;36:
669675.
116. Finkelstein MM. A study of doseresponse relationships for asbestos
associated disease. Br J Ind Med 1985;42:319325.
117. Gibbs AR, Stephens M, Griffiths DM, Blight BJN, Pooley FD. Fibre
distribution in the lungs and pleura of subjects with asbestos related
diffuse pleural fibrosis. Br J Ind Med 1991;48:762770.
118. Stephens M, Gibbs AR, Pooley FD, Wagner JC. Asbestos induced
diffuse pleural fibrosis: pathology and mineralogy. Thorax 1987;42:
583588.
119. Kee ST, Gamsu G, Blanc P. Causes of pulmonary impairment in asbestos-exposed individuals with diffuse pleural thickening. Am J Respir
Crit Care Med 1996;154:789793.
120. Green RA, Dimcheff DG. Massive bilateral upper lobe fibrosis secondary to asbestos exposure. Chest 1974;65:5255.
121. Hillerdal G. Pleural and parenchymal fibrosis mainly affecting the upper
lobes in persons exposed to asbestos. Respir Med 1990;84:129134.
122. Miller A, Teirstein AS, Selikoff IJ. Ventilatory failure due to asbestos
pleurisy. Am J Med 1983;75:911919.
123. Hanke R. Rundatelektasen (Kugel- und Walzenatelektasen): ein Beitrag zur differential diagnose intrapulmonaler Rundherde. Fortschr
Roentgenstr 1971;114:164183.
124. Hillerdal G. Rounded atelectasis: clinical experience with 74 patients.
Chest 1989;95:836841.
125. Blesovsky A. The folded lung. Br J Dis Chest 1996;60:1922.
126. Gamsu G, Aberle DR, Lynch D. Computed tomography in the diagnosis
of asbestos-related thoracic disease. J Thorac Imaging 1989;4:6167.
127. Kennedy SM, Vedal S, Muller N, Kassam A, Chan-Yeung M. Lung
function and chest radiograph abnormalities among construction insulators. Am J Ind Med 1991;20:673684.
128. Jodoin G, Gibbs GW, Macklem PT, McDonald JC, Becklake MR. Early
effects of asbestos exposure on lung function. Am Rev Respir Dis
1971;104:525535.
129. Mohsenifar Z, Jasper AJ, Mahrer T, Koerner SK. Asbestos and airflow
limitation. J Occup Med 1985;28:817820.
130. Wright JL, Churg A. Morphology of small airways disease induced by
asbestos exposure. Hum Pathol 1984;15:6874.
131. Fournier-Massey G, Becklake MR. Pulmonary function profiles in Quebec asbestos workers. Bull Physiopathol Respir (Nancy) 1975;11:429
445.
132. Rodriguez-Roisin R, Merchant JE, Cochrane GM, Hickey BP, TurnerWarwick M, Clark TJ. Maximal expiratory flow volume curves in
workers exposed to asbestos. Respiration (Herrlisheim) 1980;39:5865.
133. Wang XR, Yano E, Nonaka K, Wang M, Wang Z. Pulmonary function
of nonsmoking female asbestos workers without radiographic signs
of asbestosis. Arch Environ Health 1998;53:292298.
134. Nkadate T. Decline in annual lung function in workers exposed to
asbestos with and without pre-existing fibrotic changes on chest radiography. Occup Environ Med 1995;52:368373.
135. Wang XR, Christiani DC. Respiratory symptoms and functional status
in workers exposed to silica, asbestos, and coal mine dusts. J Occup
Environ Med 2000;42:10761084.

136. Kilburn K, Warshaw RH, Einstein K, Bernstein J. Airway disease in
non-smoking asbestos workers. Arch Environ Health 1985;40:293
295.
137. Griffith DE, Garcia JGN, Dodson RF, Levin JL, Kronenberg RS. Airflow obstruction in nonsmoking, asbestos- and mixed dust-exposed
workers. Lung 1993;171:213224.
138. Begin R, Filion R, Ostiguy G. Emphysema in silica- and asbestosexposed workers seeking compensation: CT scan study. Chest 1995;108:
647655.
139. Wright JL, Churg A. Severe diffuse small airways disease in long-term
chrysotile miners. Br J Ind Med 1985;42:556559.
140. Pinkerton KE, Green FHY, Saiki C, Vallyathan V, Plopper CG, Gopal
V, Hung D, Bahne EB, Lin SS, Menache MG, et al. Distribution of
particulate matter and tissue remodeling in the human lung. Environ
Health Perspect 2000;108:10631069.
141. Siracusa A, Forcina A, Volpi R, Mollichella E, Cicioni C, Fiordi T. An
11-year longitudinal study of the occupational dust exposure and lung
function of polyvinyl chloride, cement and asbestos cement factory
workers. Scand J Work Environ Health 1988;14:181188.
142. Schwartz DA, Davis CS, Merchant JA, Bunn WB, Galvin JR, van
Fossen DS, Dayton CS, Hunninghake GW. Longitudinal changes in
lung function among asbestos-exposed workers. Am J Respir Crit
Care Med 1994;150:12431249.
143. Dujic Z, Tocilj J, Saric M. Early detection of interstitial lung disease
in asbestos exposed non-smoking workers by mid-expiratory flow
rate and high resolution computed tomography. Br J Ind Med 1991;
48:663664.
144. Barnhart S, Hudson LD, Mason SE, Pierson DJ, Rosenstock L. Total
lung capacity: an insensitive measure of impairment in patients with
asbestosis and chronic obstructive pulmonary disease? Chest 1988;93:
299302.
145. Kilburn K, Miller A, Warshaw RH. Measuring lung volumes in advanced
asbestosis: comparability of plethysmographic and radiographic versus helium rebreathing and single breath methods. Respir Med 1993;
87:115120.
146. Wright JL, Tron V, Wiggs B, Churg A. Cigarette smoke potentiates
asbestos-induced airflow abnormalities. Exp Lung Res 1988;14:537
548.
715
147. Anonymous. Asbestos, asbestosis, and cancer: the Helsinki criteria for
diagnosis and attribution. Scand J Work Environ Health 1997;23:311
316.
148. Ohar J, Sterling DA, Bleecker E, Donohue J. Changing patterns in
asbestos-induced lung disease. Chest 2004;125:744753.
149. Osinubi Y, Afilaka AA, Doucette J, Golden A, Soriano T, Rovner E,
Anselm E. Study of smoking behavior in asbestos workers. Am J Ind
Med 2002;41:6269.
150. Ross RM. The clinical diagnosis of asbestosis in this century requires
more than a chest radiograph. Chest 2003;124:11201128.
151. Homa DM, Garabrant DH, Gillespie BW. A meta-analysis of colorectal
cancer and asbestos exposure. Am J Epidemiol 1994;139:12101222.
152. U.S. Preventive Services Task Force. Lung cancer screening: recommendation statement. Ann Intern Med 2004;140:738739.
153. Humphrey LL, Teutsch S, Johnson M. Lung cancer screening with
sputum cytologic examination, chest radiography, and computed tomography: an update for the US Preventive Services Task Force.
Ann Intern Med 2004;140:740753.
154. Goodman M, Morgan RW, Ray R, Malloy CD, Zhao K. Cancer in
asbestos-exposed occupational cohorts: a meta-analysis. Cancer Causes
Control 1999;10:453465.
155. Smith RA, Mettlin CJ, Davis KJ, Eyre H. American Cancer Society
guidelines for the early detection of cancer. CA Cancer J Clin 2000;
50:3449.
156. Seidman H, Selikoff IJ, Gelb SK. Mortality experience of amosite asbestos factory workers: doseresponse relationships 5 to 40 years after
onset of short-term work exposure. Am J Ind Med 1986;10:479514.
157. Cocchiarella L, Abdersson GBJ, editors. Guides to the evaluation of
permanent impairment. Chicago, IL: AMA Press; 2001. p. 87115.
158. Association of Occupational and Environmental Clinics. Asbestos
screening (resolution adopted Spring 2000). Available online at
www.aoec.org/asbestos-screen.htm. Accessed July 29, 2004.
159. Egilman D, Bohme SR. Attorney-directed screenings can be dangerous.
Am J Ind Med 2004;45:305307.
160. National Institute for Occupational Safety and Health. Comments to
DOL: Comments of the National Institute for Occupational Safety
and Health on the Mine Safety and Health Administration Advanced
Notice of Proposed Rulemaking on Measuring and Controlling Asbestos Exposure, 30 CFR Parts 58 and 72, 2002.

Asbestos

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Asbestos

Uploaded by

Copyright:

Available Formats

American Thoracic Society Documents

Diagnosis and Initial Management of Nonmalignant

at a subclinical level and may not be sufficiently advanced to be

DIAGNOSTIC CRITERIA AND GUIDELINES FOR

TABLE 1. CRITERIA FOR DIAGNOSIS OF NONMALIGNANT LUNG DISEASE RELATED TO ASBESTOS

Comparison and Notes

Chest film (irregular opacities)

Evidence of structural change, as

Pathology (College of American

Histology (College of American

Consistent time interval

Evidence of plausible causation, as

Evidence of plausible causation implies that the temporal

Rule out other causes of interstitial fibrosis

Exclusion of alternative diagnoses

The 1986 guidelines primarily addressed asbestosis but

Evidence of abnormal test

Evidence of functional impairment, as

Functional assessment is not required for diagnosis but is part

Occupational and environmental history

Asbestos bodies or fibers in lung tissue

Crackles, bilateral, not cleared by cough

Reduced diffusing capacity

Change in ventilatory function (restrictive,

Demonstrates the existence of a structural lesion consistent

The 2004 guidelines are not limited to lung tissue, consider

The 1986 guidelines noted possible utility of bronchoalveolar

The generic term asbestos is used to describe a group of

the National Research Council (1), the term asbestos is a

American Thoracic Society Documents

one another. Commercial asbestos has high tensile strength,

Asbestos fibers carried to the deep lung induce an alveolitis that

Figure 1. Low-power photomicrograph of hematoxylin and

the presence of a large iron peak signifies an amphibole (with

American Thoracic Society Documents

been coated with an iron-rich, proteinaceous concretion (Figures

CLINICAL EVALUATION AND INDICATORS

The insidious onset of dyspnea is the most common respiratory

capacity has been observed for cough, phlegm, and symptoms

graphic findings (33). These findings established that sheet metal

The chest radiograph remains an extremely useful tool for the

requires conventional film-based posteroanterior (PA) chest

A chest film clearly showing the characteristic signs of asbestosis

American Thoracic Society Documents

significance. HRCT is more specific than plain chest radiographs,

no crocidolite detected. BAL performed on asbestos-exposed

Evaluation of subjects with suspected asbestos-related disease

NONMALIGNANT DISEASE OUTCOMES

Asbestosis is the interstitial pneumonitis and fibrosis caused by

Figure 3. H&E-stained section

Figure 4. H&E-stained section

American Thoracic Society Documents

Figure 6. H&E-stained section

Developed in 1980 by a committee of the College of American Pathologists.

Iron stains may facilitate recognition of the asbestos bodies;

duration and intensity of exposure probably influence the length

American Thoracic Society Documents

diagnosis of asbestosis when a significant exposure history is

Figure 7. Whole lung section of freeze-dried lung from a person who

terized physiologically by increased isoflow volume, and increased

Figure 9. Early asbestosis, showing irregular opacities in lower lung

Pleural abnormalities associated with asbestos exposure are the

American Thoracic Society Documents

Figure 10. Photomicrograph of H&E-stained section of lung